HCSGD entry for BMI1
1. General information
| Official gene symbol | BMI1 |
|---|---|
| Entrez ID | 648 |
| Gene full name | BMI1 polycomb ring finger oncogene |
| Other gene symbols | FLVI2/BMI1 PCGF4 RNF51 |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000122 | Negative regulation of transcription from RNA polymerase II promoter | IMP | biological_process |
| GO:0000151 | Ubiquitin ligase complex | IDA | cellular_component |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005634 | Nucleus | IDA | cellular_component |
| GO:0005730 | Nucleolus | IDA | cellular_component |
| GO:0005737 | Cytoplasm | IEA | cellular_component |
| GO:0006351 | Transcription, DNA-templated | IEA | biological_process |
| GO:0007379 | Segment specification | TAS | biological_process |
| GO:0008270 | Zinc ion binding | IDA IEA | molecular_function |
| GO:0010468 | Regulation of gene expression | IMP | biological_process |
| GO:0016568 | Chromatin modification | IEA | biological_process |
| GO:0030097 | Hemopoiesis | IEP | biological_process |
| GO:0031519 | PcG protein complex | IDA | cellular_component |
| GO:0035102 | PRC1 complex | IDA | cellular_component |
| GO:0048146 | Positive regulation of fibroblast proliferation | IMP | biological_process |
| GO:0051443 | Positive regulation of ubiquitin-protein ligase activity | IDA | biological_process |
| GO:0071535 | RING-like zinc finger domain binding | IPI | molecular_function |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.9193481935 | 0.6301503932 | 0.9999902473 | 1.0000000000 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
| Data source | Up or down | Log fold change |
|---|---|---|
| GSE11954 | - | - |
| GSE13712_SHEAR | - | - |
| GSE13712_STATIC | - | - |
| GSE19018 | - | - |
| GSE19899_A1 | - | - |
| GSE19899_A2 | - | - |
| PubMed_21979375_A1 | - | - |
| PubMed_21979375_A2 | - | - |
| GSE35957 | - | - |
| GSE36640 | - | - |
| GSE54402 | - | - |
| GSE9593 | - | - |
| GSE43922 | - | - |
| GSE24585 | - | - |
| GSE37065 | - | - |
| GSE28863_A1 | Down | -0.3708900300 |
| GSE28863_A2 | Down | -0.1187103140 |
| GSE28863_A3 | Up | 0.1658372492 |
| GSE28863_A4 | Up | 0.0070344867 |
| GSE48662 | Up | 0.1173619746 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-200c-3p | MIMAT0000617 | MIRT000197 | Luciferase reporter assay//Western blot | Functional MTI | 19665978 |
| hsa-miR-200c-3p | MIMAT0000617 | MIRT000197 | Immunoblot//Luciferase reporter assay//qRT-PCR | Functional MTI | 21294122 |
| hsa-miR-200c-3p | MIMAT0000617 | MIRT000197 | Luciferase reporter assay//Northern blot//qRT-PCR//Western blot | Functional MTI | 21207483 |
| hsa-miR-16-5p | MIMAT0000069 | MIRT000266 | Luciferase reporter assay//Western blot | Functional MTI | 19903841 |
| hsa-miR-15a-5p | MIMAT0000068 | MIRT000280 | Luciferase reporter assay//Western blot | Functional MTI | 19903841 |
| hsa-miR-128-3p | MIMAT0000424 | MIRT004645 | Immunohistochemistry//In situ hybridization//Microarray//qRT-PCR//Western blot | Functional MTI | 19010882 |
| hsa-miR-128-3p | MIMAT0000424 | MIRT004645 | Luciferase reporter assay//Western blot | Functional MTI | 20574517 |
| hsa-miR-128-3p | MIMAT0000424 | MIRT004645 | Northern blot//Western blot | Functional MTI | 19941032 |
| hsa-miR-302b-3p | MIMAT0000715 | MIRT005670 | Luciferase reporter assay//Microarray//Northern blot//Western blot | Functional MTI | 21062975 |
| hsa-miR-194-5p | MIMAT0000460 | MIRT007000 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 21851624 |
| hsa-miR-218-5p | MIMAT0000275 | MIRT007258 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 23255074 |
| hsa-let-7g-5p | MIMAT0000414 | MIRT024120 | Western blot;qRT-PCR | Functional MTI | 20309945 |
| hsa-miR-33a-5p | MIMAT0000091 | MIRT028182 | Sequencing | Functional MTI (Weak) | 20371350 |
| hsa-miR-106b-3p | MIMAT0004672 | MIRT038596 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-27a-3p | MIMAT0000084 | MIRT050022 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
MicroRNA name | mirBase ID | Target site number | MiRNA mature ID | Test method inter | MiRNA regulation site | Reporter target site | Pubmed ID |
|---|---|---|---|---|---|---|---|
| hsa-miR-15a-5p | MIMAT0000068 | 1 | hsa-miR-15a | {Western blot} | {overexpression by miRNA precursor transfection} | 19903841 | |
| hsa-miR-16-5p | MIMAT0000069 | 1 | hsa-miR-16 | {Western blot} | {overexpression by miRNA precursor transfection} | 19903841 | |
| hsa-miR-16-5p | MIMAT0000069 | 2 | hsa-miR-16 | {Western blot} | {overexpression by miRNA precursor transfection} | 19903841 | |
| hsa-miR-200b-3p | MIMAT0000318 | NA | hsa-miR-200b | {Western blot} | {overexpression by miRNA mimics tranfection} | 21725369 | |
| hsa-miR-15b-5p | MIMAT0000417 | NA | hsa-miR-15b | {Western blot} | {overexpression by miRNA mimics tranfection} | 21725369 | |
| hsa-miR-708-5p | MIMAT0004926 | 1 | hsa-miR-708 | 21852381 | |||
| hsa-miR-302b-3p | MIMAT0000715 | 1 | hsa-miR-302b | {Western blot} | {overexpression by miRNA mimics tranfection} | 21062975 | |
| hsa-miR-302b-3p | MIMAT0000715 | 2 | hsa-miR-302b | {Western blot} | {overexpression by miRNA mimics tranfection} | 21062975 |
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6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 58 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 27228653 | Bmi1 supports SSC via transcriptional suppression of genes associated with cell cycle and differentiation |
| 27228653 | The most studied target genes of Bmi1 are the genes of Ink4 locus, CdkI p16(Ink4a) and p1(Arf), suppression of which due to activating mutations of the BMI1 results in formation of cancer stem cells (CSC) and carcinomas in various tissues |
| 27228653 | In contrast, inactivation of BMI1 results in cell cycle arrest and cell senescence |
| 27228653 | Although clinical phenomena of hypo- and hyperactivation of BMI1 are well known, its targets and mechanisms of regulation of tissue specific SSC are still obscure |
| 27228653 | The goal of this study was to evaluate the regulatory role of BMI1 in adipocyte differentiation (AD) of mouse mesenchymal stem cells (MSC) |
| 27228653 | Induction of AD in mouse MSC of the C3H10T1/2 cell line was associated with an increase in the expression levels of BMI1, the genes of pRb family (RB, p130) and demethylase UTX, but not methyltransferase EZH2, whose products regulate the methylation levels of H3K27 |
| 27228653 | Here we show that inactivation of BMI1 using specific siRNA slows and decreases the levels of AD, but does not abolish it |
| 27105531 | A miR-200c/141-BMI1 autoregulatory loop regulates oncogenic activity of BMI1 in cancer cells |
| 27105531 | The miR-200c/141 locus on chromosome 12 encodes miR-200c and miR-141, two members of the miR-200 family, which have been shown to function as tumor suppressive miRNAs by targeting multiple oncogenic factors such as polycomb group protein BMI1 |
| 27105531 | Here, we show that BMI1 reciprocally functions as a transcriptional repressor of the miR-200c/141 cluster and that BMI1 inhibitors upregulate expression of miR-200c and miR-141 |
| 27105531 | Our data suggest that BMI1 binds to the miR-200c/141 promoter and regulates it through transcription factor binding motifs E-box 2 and Z-box 1 to repress expression of miR-200c/141 cluster |
| 27105531 | We also show that PTC-209, a small molecule inhibitor of BMI1 gene expression induces cellular senescence and transcriptionally upregulates expression of miR-200c/141 cluster in breast cancer cells |
| 27105531 | Therefore, our studies suggest a reciprocal regulation between BMI1 and miR-200c/141 cluster, and that BMI1 inhibitory drugs can further amplify their inhibitory effects on BMI1 via multiple mechanisms including posttranscriptional regulation by upregulating BMI1 targeting miRNAs |
| 27009837 | Antitumor activity and inhibitory effects on cancer stem cell-like properties of Adeno-associated virus (AAV) -mediated Bmi-1 interference driven by Bmi-1 promoter for gastric cancer |
| 27009837 | Bmi-1 is aberrantly activated in various cancers and plays a vital role in maintaining the self-renewal of stem cells |
| 27009837 | Our previous research revealed that Bmi-1 was overexpressed in gastric cancer (GC) and it's overexpression was an independent negative prognostic factor, suggesting it can be a therapeutic target |
| 27009837 | The main purpose of this investigation was to explore the antitumor activity of Bmi-1 interference driven by its own promoter (Ad-Bmi-1i) for GC |
| 27009837 | In this study, we used adenoviral vector to deliver Bmi-1 shRNA driven by its own promoter to treat GC |
| 27009837 | Our results revealed that Ad-Bmi-1i could selectively silence Bmi-1 in GC cells which overexpress Bmi-1 and suppress the malignant phenotypes and stem-like properties of GC cells in vitro and in vivo |
| 27009837 | Bmi-1 knockdown by Ad-Bmi-1i downregulated VEGF via inhibiting AKT activity |
| 26941359 | In addition, CD146 suppression in hUCB-MSCs caused downregulation of other cellular senescence regulators, including Bmi-1, Id1, and Twist1 |
| 26640145 | In CTCL cells expressing wild-type p53, forced expression of miR-16 enhanced p21 expression via downregulation of the polycomb group protein Bmi1, thereby inducing cellular senescence |
| 26573462 | Senescence-Associated MCP-1 Secretion Is Dependent on a Decline in BMI1 in Human Mesenchymal Stromal Cells |
| 26573462 | Moreover, BMI1, a polycomb protein, repressed the expression of MCP-1 by binding to its regulatory elements |
| 26573462 | The reduction in BMI1 levels during UCB-MSC senescence altered the epigenetic status of MCP-1, including the loss of H2AK119Ub, and resulted in derepression of MCP-1 |
| 26573462 | CONCLUSION: Senescence of UCB-MSCs is orchestrated by MCP-1, which is secreted as a major component of the SASP and is epigenetically regulated by BMI1 |
| 26238021 | BMI1 polycomb ring finger oncogene (Bmi1) is an oncogene associated with radioresistance in tumor cells |
| 26238021 | MicroRNA (miRNA)128a is a brain-specific miRNA, which suppresses Bmi1 expression |
| 26238021 | The mRNA expression levels of Bmi1 and those of miRNA128a in U87 MG cells exposed to Xray radiation were evaluated by reverse transcriptionquantitative polymerase chain reaction |
| 26238021 | The mRNA expression levels of Bmi1 were downregulated in the 1 and 2 Gy groups, and upregulated in the 6 and 8 Gy groups |
| 26238021 | High doses of Xray radiation increased the expression levels of Bmi1, which may be associated with the evasion of cellular senescence |
| 25832744 | Bmi-1 prevents stem cell aging, at least partly, by blocking expression of the cyclin-dependent kinase inhibitor p16(Ink4a) |
| 25832744 | However, because Bmi-1 knockout (KO) mice die within 20 weeks after birth, it is difficult to determine exactly where and when dysregulation of the Bmi-1/p16(Ink4a) pathway occurs during aging in vivo |
| 25737447 | The up-regulation of miR-31 was accompanied by repression of the polycomb group (PcG) protein BMI1 and induction of cellular senescence |
| 25737447 | We further show that inhibition of miR-31 overcomes the senescence-inducing effect of HDACi, and restores expression of the PcG protein BMI1 |
| 25737447 | Interestingly, BMI1 also acts as a repressor of miR-31 transcription, suggesting a cross-negative feedback loop between the expression of miR-31 and BMI1 |
| 25505268 | PLK1 inhibition down-regulates polycomb group protein BMI1 via modulation of the miR-200c/141 cluster |
| 25505268 | The polycomb group protein BMI1 is an important regulator of cancer stem cell (CSC) phenotype and is often overexpressed in cancer cells |
| 25505268 | BMI1 functions via polycomb repressive complex 1 (PRC1)-mediated gene silencing and also via PRC1-independent transcriptional activities |
| 25505268 | At present, very little is known about the therapy reagents that can efficiently inhibit BMI1 expression, and the CSC phenotype |
| 25505268 | Here, we report that the polo-like kinase 1 (PLK1) regulates BMI1 expression, and that its inhibition can efficiently down-regulate BMI1 expression and PRC1 activity, and induce premature senescence in breast cancer cells |
| 25505268 | We also show that the exogenous BMI1 overexpression mitigates anti-oncogenic effects of PLK1 inhibition and overcomes senescence induction by PLK1 inhibitors |
| 25505268 | We further show that PLK1 inhibition down-regulates BMI1 by upregulating the miRNA-200c/141 cluster, which encodes miR-200c and miR-141, both of which are known to post-transcriptionally downregulate BMI1 expression |
| 25505268 | Thus, our data suggest that PLK1 inhibitors can be successfully used to inhibit growth of tumors in which PcG protein BMI1 is overexpressed or the PRC1 activity is deregulated |
| 25485497 | Here we discuss on how cellular senescence may be a common mechanism of stem cell aging at the organism level and show that induction of p16(INK4a) in young muscle stem cells through deletion of the Polycomb complex protein Bmi1 recapitulates the geriatric phenotype |
| 25364434 | Bmi-1 induces radioresistance by suppressing senescence in human U87 glioma cells |
| 25364434 | Bmi-1 has been proposed to be an oncogene that can induce anti-senescence in tumor cells |
| 25364434 | The present study investigated the response of U87 glioma cells to radiation exposure and the role of Bmi-1 in the response following radiotherapy |
| 25364434 | Following exposure to radiation, the cell cycle distribution was dysregulated, with an increased number of cells in the G2/M phase, and the expression of Bmi-1 was upregulated, particularly when a dose of >/=6 Gy was administered |
| 25364434 | In addition, Bmi-1 may be significant in increasing the radioresistance of glioma cells by enabling cell senescence |
| 25263442 | The Polycomb group protein Bmi-1 is an essential regulator of cellular senescence and is believed to function largely through the direct repression of the Ink4a/Arf locus |
| 25263442 | However, concurrent deletion of Ink4a/Arf does not fully rescue the defects detected in Bmi-1(-/-) mice, indicating that additional Bmi-1 targets remain to be identified |
| 25263442 | Here we demonstrate that oncogenic stress leads to the dissociation of Bmi-1 from the Sin3B locus, resulting in increased Sin3B expression and subsequent entry into cellular senescence |
| 25263442 | Furthermore, Sin3B is required for the senescent phenotype and elevated levels of reactive oxygen species elicited upon Bmi-1 depletion |
| 25263442 | Altogether, these results identify Sin3B as a novel direct target of Bmi-1, and establish Bmi-1-driven repression of Sin3B as an essential regulator of cellular senescence |
| 25224681 | Decline in the gene expression of senescence repressor Bmi1, and telomerase, together with telomere shortening, underlay senescence of stem cells cultured for multiple passages |
| 25224681 | After a 90-day culture, REAC-treated cells exhibited significantly higher transcription of Bmi1 and enhanced expression of other stem cell pluripotency genes and related proteins, compared to unexposed cells |
| 25057072 | OBJECTIVE: To investigate the effect of silencing Bmi-1 expression in reversing cisplatin resistance in human lung cancer cells and explore the possible mechanisms |
| 25057072 | METHODS: Cisplatin-resistant A549/DDP cells with small interference RNA (siRNA)-mediated Bmi-1 expression silencing were examined for cisplatin sensitivity using MTT assay and alterations in cell cycle distribution and apoptosis with flow cytometry, and the changes in cell senescence was assessed using beta-galactosidase staining |
| 25057072 | RESULTS: A549/DDP cells showed significantly higher Bmi-1 expression than A549 cells |
| 25057072 | After siRNA-mediated Bmi-1 silencing, A549/DDP cells showed significantly enhanced cisplatin sensitivity with an increased IC50 from 40 |
| 25057072 | CONCLUSION: Silencing Bmi-1 by RNA interference can induce cell senescence and resensitize A549/DDP cells to cisplatin possibly by regulating INK4a/ARF/Rb senescence pathway |
| 24853424 | In addition, we show that WIF1 functions as a positive regulator of miR-200c, leading to downregulation of BMI1, ZEB1 and ZEB2, with a consequent increase in downstream targets such as E-cadherin |
| 24379598 | Silencing Bmi-1 enhances the senescence and decreases the metastasis of human gastric cancer cells |
| 24379598 | METHODS: Two pairs of complementary small hairpin RNA (shRNA) oligonucleotides targeting the Bmi-1 gene were designed, synthesized, annealed and cloned into the pRNAT-U6 |
| 24379598 | The expression of Bmi-1 mRNA and protein was examined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting |
| 24379598 | The effects of Bmi-1 knockdown on cell senescence and metastasis were determined by the beta-Gal activity assay and Boyden chamber assay, respectively |
| 24379598 | RESULTS: The double-stranded oligonucleotide fragments of Bmi-1 short interfering RNA (siRNA) cloned into pRNAT-U6 |
| 24379598 | RT-PCR and Western blotting indicated that the expression levels of Bmi-1 gene mRNA and protein were markedly decreased in transfected BGC823 cells with pRNAT-U6 |
| 24379598 | In particular, Bmi-1 protein expression was almost completely abolished in cells transfected with the recombinant vector harboring shRNA targeting the sequence GGAGGAGGTGAATGATAAA (nt1104-1122) |
| 24379598 | CONCLUSION: Silencing Bmi-1 by RNA interference can increase the senescent cell rate and effectively reduce the metastasis of gastric cancer cells |
| 23468063 | Copper induces cellular senescence in human glioblastoma multiforme cells through downregulation of Bmi-1 |
| 23468063 | We further demonstrated that the Bmi-1 pathway was downregulated in GBM cells in parallel with the induced senescence |
| 23468063 | The present study for the first time demonstrates the ability of copper to induce GBM cell senescence by downregulating Bmi-1 |
| 22554522 | Combined introduction of Bmi-1 and hTERT immortalizes human adipose tissue-derived stromal cells with low risk of transformation |
| 22554522 | To this end, combinations of human telomerase reverse transcriptase (hTERT), murine Bmi-1, and SV40 large T antigen (SV40T) were introduced by lentiviral transduction into ASCs |
| 22554522 | The combination of Bmi-1 and hTERT successfully immortalized human ASCs without significantly perturbing their phenotype or biological behavior |
| 22509111 | High expression of p16INK4a and low expression of Bmi1 are associated with endothelial cellular senescence in the human cornea |
| 22509111 | PURPOSE: Determine cyclin-dependent kinase inhibitor 2A (p16(Ink4a)) and polycomb ring finger oncogene (Bmi1) expression in corneal endothelium samples from different age groups and test whether the expression of p16(INK4a) and Bmi1 are associated with endothelial cellular senescence in human cornea |
| 22509111 | RESULTS: Through real-time PCR, we detected less than threefold decreases in Bmi1 expression and greater than fivefold increases in p16(INK4a) expression associated with aging |
| 22509111 | Bmi1 expression was significantly down-regulated with increasing donor age |
| 22509111 | Our immunohistochemistry experiments showed that the expression of p16(INK4a) in older donors was stronger than that in younger donors and the expression of Bmi1 in older donors was weaker than that in younger donors |
| 22509111 | Results from both the immunohistochemistry and real-time PCR experiments confirmed increased expression of p16(INK4a) and decreased expression of Bmi1 with age in HCECs |
| 22509111 | Additionally, the results of immunofluorescence double-staining for p16(INK4a) and Bmi1 further validated the immunocytochemistry and real-time PCR results |
| 22509111 | CONCLUSIONS: Our data are the first to demonstrate that high expression of p16(INK4a) and low expression of Bmi1 are associated with endothelial cellular senescence in human cornea |
| 22363787 | Bmi-1 absence causes premature brain degeneration |
| 22363787 | Bmi-1, a polycomb transcriptional repressor, is implicated in cell cycle regulation and cell senescence |
| 22363787 | Here, we demonstrate the occurrence of oxidative stress in the brain of four-week-old Bmi-1 null mice |
| 22363787 | Moreover, astroglial glutamate transporters and glutamine synthetase decreased in the Bmi-1 null hippocampus, which might contribute to the sporadic epileptic-like seizures in these mice |
| 22363787 | These results indicate that Bmi-1 is required for maintaining endogenous antioxidant defenses in the brain, and its absence subsequently causes premature brain degeneration |
| 21624810 | Functional crosstalk between Bmi1 and MLL/Hoxa9 axis in establishment of normal hematopoietic and leukemic stem cells |
| 21624810 | Bmi1 is required for efficient self-renewal of hematopoietic stem cells (HSCs) and leukemic stem cells (LSCs) |
| 21624810 | In this study, we investigated whether leukemia-associated fusion proteins, which differ in their ability to activate Hox expression, could initiate leukemia in the absence of Bmi1 |
| 21624810 | As reported for Bmi1, Hoxa9 regulates expression of p16(Ink4a)/p19(ARF) locus and could overcome senescence induced by AML1-ETO |
| 21624810 | Together, these results reveal an important functional interplay between MLL/Hox and Bmi1 in regulating cellular senescence for LSC development, suggesting that a synergistic targeting of both molecules is required to eradicate a broader spectrum of LSCs |
| 21572997 | DNA methyltransferase controls stem cell aging by regulating BMI1 and EZH2 through microRNAs |
| 21559395 | Consistent with this hypothesis, EWS-FLI1 induced hNCSC genes as well as the polycomb proteins BMI-1 and EZH2 in hNC-MSC |
| 21559395 | In addition, up-regulation of BMI-1 was associated with avoidance of cellular senescence and reversible silencing of p16 |
| 21559395 | In addition, to our knowledge this is the first demonstration that EWS-FLI1-mediated induction of BMI-1 and epigenetic silencing of p16 might be critical early initiating events in ESFT tumorigenesis |
| 21430439 | The polycomb group protein BMI1 has been linked to proliferation, senescence, cancer progression and stem cell phenotype |
| 21430439 | Here, we report that BMI1 contains a functional recognition motif for the F box protein betaTrCP, which regulates ubiquitination and proteasome-mediated degradation of various proteins |
| 21430439 | We show that overexpression of wild-type betaTrCP but not the DeltaF mutant of it promotes BMI1 ubiquitination and degradation, and knockdown of betaTrCP results in increased expression of BMI1 |
| 21430439 | Furthermore, a mutant of BMI1 with an altered betaTrCP recognition motif is much more stable than wild-type BMI1 |
| 21430439 | We also show that wild-type BMI1 but not the mutant BMI1 interacts with betaTrCP |
| 21430439 | Accordingly, compared to wild-type BMI1, mutant protein exhibited increased pro-oncogenic activity |
| 21430439 | In summary, our findings suggest that betaTrCP regulates turnover of BMI1 and its function relevant to oncogenesis, cellular senescence and aging |
| 20808772 | METHODOLOGY/PRINCIPAL FINDINGS: We examined the function of Zinc finger domain-containing protein 277 (Zfp277), a novel zinc finger protein that interacts with the PcG protein Bmi1 |
| 20808772 | Zfp277 binds to the Ink4a/Arf locus in a Bmi1-independent manner and interacts with polycomb repressor complex (PRC) 1 through direct interaction with Bmi1 |
| 20808772 | Notably, forced expression of Bmi1 in Zfp277(-/-) MEFs did not restore the binding of Bmi1 to the Ink4a/Arf locus and failed to bypass cellular senescence |
| 20808772 | A Zfp277 mutant that could not bind Bmi1 did not rescue Zfp277(-/-) MEFs from premature senescence |
| 20808772 | CONCLUSIONS/SIGNIFICANCE: Our findings implicate Zfp277 in the transcriptional regulation of the Ink4a/Arf locus and suggest that the interaction of Zfp277 with Bmi1 is essential for the recruitment of PRC1 to the Ink4a/Arf locus |
| 20652278 | Consistently, the expression of Bmi1, which prevents hematopoietic progenitor cell senescence, was significantly reduced in diabetic bone marrow cells |
| 20574517 | MicroRNA 128a increases intracellular ROS level by targeting Bmi-1 and inhibits medulloblastoma cancer cell growth by promoting senescence |
| 20574517 | One of these, miR-128a, inhibits growth of medulloblastoma cells by targeting the Bmi-1 oncogene |
| 20574517 | CONCLUSIONS AND SIGNIFICANCE: Here we report the novel regulation of reactive oxygen species (ROS) by microRNA 128a via the specific inhibition of the Bmi-1 oncogene |
| 20574517 | We demonstrate that miR-128a has growth suppressive activity in medulloblastoma and that this activity is partially mediated by targeting Bmi-1 |
| 20569464 | Deletion analysis of BMI1 oncoprotein identifies its negative regulatory domain |
| 20569464 | BACKGROUND: The polycomb group (PcG) protein BMI1 is an important regulator of development |
| 20569464 | Additionally, aberrant expression of BMI1 has been linked to cancer stem cell phenotype and oncogenesis |
| 20569464 | Despite its established role in stem cell maintenance, cancer and development, at present not much is known about the functional domains of BMI1 oncoprotein |
| 20569464 | In the present study, we carried out a deletion analysis of BMI1 to identify its negative regulatory domain |
| 20569464 | RESULTS: We report that deletion of the C-terminal domain of BMI1, which is rich in proline-serine (PS) residues and previously described as PEST-like domain, increased the stability of BMI1, and promoted its pro-oncogenic activities in human mammary epithelial cells (HMECs) |
| 20569464 | Furthermore, when compared to the wild type BMI1, exogenous expression of the mutant BMI1 led to a significant downregulation of p16INK4a and an efficient bypass of cellular senescence in human diploid fibroblasts |
| 20569464 | CONCLUSIONS: In summary, our data suggest that the PS domain of BMI1 is involved in its stability and that it negatively regulates function of BMI1 oncoprotein |
| 20569464 | Our results also suggest that the PS domain of BMI1 could be targeted for the treatment of proliferative disorders such as cancer and aging |
| 20551323 | Bmi-1, the first functionally identified polycomb gene family member, plays critical roles in cell cycle regulation, cell immortalization, and cell senescence |
| 20551323 | Bmi-1 is involved in the development and progression of carcinomas and is a potent target for cancer therapy |
| 20551323 | One important pathway regulated by Bmi-1 is that involving two cyclin-dependent kinase inhibitors, p16(Ink4a) and p19(Arf), as Bmi-1 represses the INK4a locus on which they are encoded |
| 20551323 | A close correlation between the up-regulation of Bmi-1 and down-regulation of p16 has been demonstrated in various tumors; however, how Bmi-1 regulates p16 expression is not clear |
| 20551323 | In this study, we revealed that Bmi-1 regulates the expression of p16 by binding directly to the Bmi-1-responding element (BRE) within the p16 promoter |
| 20551323 | Chromatin immunoprecipitation sequencing of Bmi-1-precipitated chromatin DNA revealed that 1536 genes were targeted by Bmi-1, including genes involved in tissue-specific differentiation, cell cycle, and apoptosis |
| 20551323 | Taken together, our results revealed the molecular mechanism of Bmi-1-mediated regulation of the p16 gene, thus providing further insights into the functions of Bmi-1 as well as a sensitive high-throughput platform with which to screen Bmi-1-targeted small molecules for cancer therapy |
| 20049504 | Decreased expression of histone deacetylases (HDACs), followed by downregulation of polycomb group genes (PcGs), such as BMI1, EZH2 and SUZ12, and by upregulation of jumonji domain containing 3 (JMJD3), was observed in senescent MSCs |
| 19907431 | Bmi-1 reduction plays a key role in physiological and premature aging of primary human keratinocytes |
| 19907431 | Analysis of the expression and activity of p16(INK4a) regulators showed that stem cell depletion, reduced proliferation, and p16(INK4a) upregulation in keratinocytes derived from the chronologically and prematurely aged epidermis strongly correlate with Bmi-1 downregulation |
| 19907431 | Our findings demonstrated that Bmi-1 is downregulated in human keratinocytes during both in vitro processes, in parallel with p16(INK4a) upregulation and accomplishment of clonal conversion |
| 19907431 | Finally, Bmi-1 overexpression reduced p16(INK4a) promoter activity and decreased protein expression in aged and diseased keratinocytes, inducing a delay of clonal conversion and an increase of cell clonogenic ability |
| 19907431 | Altogether these findings underline a key role of Bmi-1 downregulation in enforcing aging in primary human keratinocytes |
| 19695678 | Polycomb group protein Bmi1 is overexpressed and essential in anchorage-independent colony formation, cell proliferation and repression of cellular senescence in cholangiocarcinoma: tissue and culture studies |
| 19695678 | Polycomb-group proteins Bmi1 is regarded as a "stemness" gene involved in the maintenance of stem cells, malignant transformation, and biologic aggressiveness of several human carcinomas |
| 19695678 | We examined the significance of the Bmi1 expression in intrahepatic cholangiocarcinoma |
| 19695678 | The expression of Bmi1 was examined in intrahepatic cholangiocarcinoma (n = 30; 9 bile ductular carcinoma, 8 intrahepatic cholangiocarcinoma of peripheral type, and 13 of hilar type) by using immunohistochemistry and real-time polymerase chain reaction |
| 19695678 | The expression level of Bmi1 was assessed in 7 cholangiocarcinoma cell lines |
| 19695678 | The effect of Bmi1 knockdown was examined in cultured cholangiocarcinoma cells (HuCCT1 and TFK-1) using small interfering RNA |
| 19695678 | Bmi1 was consistently expressed in nonneoplastic biliary epithelial cells and in all intrahepatic cholangiocarcinoma, irrespective of the location and histological degree of differentiation |
| 19695678 | All 7 cultured cholangiocarcinoma cells overexpressed Bmi1 to various degrees |
| 19695678 | The knockdown of Bmi1 resulted in decreased colony formation, decreased cell proliferation activities, and increased cellular senescence |
| 19695678 | The overexpression of polycomb-group protein Bmi1 is essential for colony formation and cell proliferation, probably by the repression of cellular senescence in intrahepatic cholangiocarcinoma |
| 19636380 | Using tandem affinity purification, we find that CBX7 and CBX8, two Polycomb (Pc) homologs that repress INK4a, both participate in PRC1-like complexes with at least two Posterior sex combs (Psc) proteins, MEL18 and BMI1 |
| 19636380 | In primary human fibroblasts, CBX7, CBX8, MEL18 and BMI1 are present at the INK4a locus and shRNA-mediated knockdown of any one of these components results in de-repression of INK4a and proliferative arrest |
| 19578716 | Bmi-1, stem cells and cancer |
| 19578716 | Bmi-1, a polycomb gene family member, plays an important role in cell cycle regulation, cell immortalization, and cell senescence |
| 19578716 | Recently, numerous studies have demonstrated that Bmi-1 is involved in the regulation of self-renewal and differentiation of stem cells |
| 19578716 | In the present review, we summarized the function of Bmi-1 as a transcriptional regulator of gene expression, with particular reference to stem cells |
| 19318942 | Molecular analyses identified the role of sirtuin 1 in preventing cell senescence; shed light on the role of polycomb group (PcG) protein Bmi-1 in senescence |
| 19208841 | Ras expression dissociates BMI1 from the p16 locus, whereas both CUL4 and MLL1 bind to the p16 locus similarly in both normal and oncogenic stimulated cells |
| 20232599 | Stem cell divisions controlled by the proto-oncogene BMI-1 |
| 20232599 | This is exemplified by the proto-oncogene BMI-1 that is involved in the maintenance of somatic stem cells and in carcinogenesis within the same tissues |
| 20232599 | BMI-1 interferes with the central cellular tumor suppressor pathways linked to retinoblastoma protein (Rb) and p53 |
| 18948382 | Knocking down p21 via shRNA, or suppression of the p16/pRb pathway by either BMI1 or HPV16-E7 overexpression, was also insufficient to prevent hyperoxia-induced senescence |
| 18592462 | Overexpression of BMI1, a polycomb group repressor protein, in bladder tumors: a preliminary report |
| 18592462 | INTRODUCTION: A Polycomb group repressor protein named BMI1 represses the genes that induce cellular senescence and cell death, and it can contribute to cancer when improperly expressed |
| 18592462 | We aimed to evaluate expression of BMI1 gene in bladder tumors |
| 18592462 | Specific primers for BMI1 and B2M (as an internal control) were used for reverse transcript polymerase chain reaction technique |
| 18592462 | The production and distribution of BMI1 protein was also examined by western blotting and immunohistochemistry techniques |
| 18592462 | RESULTS: Polymerase chain reaction generated a 683-bp product, corresponding to the expected size of BMI1 amplified region |
| 18592462 | The mean of expression of BMI1 detected in tumor tissues was significantly higher than that in intact tissues, and there was also a significant association between the mean of gene expression and the stage of malignancy (P < |
| 18592462 | The expression of BMI1 at protein level was further confirmed by western blotting and immunohistochemistry |
| 18592462 | CONCLUSION: BMI1 is a potent repressor of retinoblastoma and p53 pathways, and hence, elucidating its role in tumorigenesis is very important |
| 18592462 | We reported for the first time the expression of BMI1 and its correlation with incidence and progress of bladder tumors |
| 17981205 | Superimposed on this basic scheme are a shift in the CD8(+) T cell response to type I and II interferon (IFN) from anti- to pro-proliferative and transcriptional control of replicative senescence by Bmi-1, Blimp-1, and BCL6/BCL6b |
| 17761140 | The sphere cells showed stem-like properties with the ability to self-renew, and expressed the stem cell-related STAT3 and Bmi1 genes |
| 17344414 | Here, we show that the ability of the oncogene BMI1 to repress the INK4A-ARF locus requires its direct association and is dependent on the continued presence of the EZH2-containing Polycomb-Repressive Complex 2 (PRC2) complex |
| 17344414 | Significantly, EZH2 is down-regulated in stressed and senescing populations of cells, coinciding with decreased levels of associated H3K27me3, displacement of BMI1, and activation of transcription |
| 17151361 | Mel-18, a polycomb group protein, regulates cell proliferation and senescence via transcriptional repression of Bmi-1 and c-Myc oncoproteins |
| 17151361 | Polycomb group (PcG) protein Bmi-1 is an important regulator of cell proliferation |
| 17151361 | Here, we report that Mel-18, a PcG ring finger protein (PCGF) transcriptionally down-regulates Bmi-1 |
| 17151361 | Furthermore, the expression of Bmi-1 and Mel-18 inversely correlates in proliferating and senescent human fibroblasts |
| 17151361 | Bmi-1 down-regulation by Mel-18 results in accelerated senescence and shortening of the replicative life span in normal human cells |
| 17151361 | Importantly, using promoter-reporter, chromatin immunoprecipitation, and quantitative real-time primary transcript RT-PCR assays, and an RNA interference approach, we demonstrate that Bmi-1 is a bona fide target of c-Myc oncoprotein |
| 17151361 | Finally, our data suggest that Mel-18 regulates Bmi-1 expression during senescence via down-regulation of c-Myc |
| 17145814 | Dysregulated expression of stem cell factor Bmi1 in precancerous lesions of the gastrointestinal tract |
| 17145814 | Polycomb protein Bmi1, which is a potent negative regulator of the p16INK4 gene, suppresses senescence in primary cells and is overexpressed in various cancers |
| 17145814 | We hypothesized that Bmi1 expression would also be dysregulated in precancerous lesions in human digestive precancerous tissues |
| 17145814 | EXPERIMENTAL DESIGN: Bmi1 expression was investigated in cancerous and precancerous tissues of the digestive tract |
| 17145814 | RESULTS: Bmi1 was clearly overexpressed across a broad spectrum of gastrointestinal cancers, and the expression of Bmi1 increased in a manner that reflected the pathologic malignant features of precancerous colonic tissues (low-grade dysplasia, 12 |
| 17145814 | CONCLUSIONS: Bmi1 overexpression was correlated with the malignant grades of human digestive precancerous tissues, which suggests that advanced Bmi1 dysregulation might predict malignant progression |
| 17145814 | The abnormal Bmi1 expression might link to malignant transformation via the disturbance of orderly histone modification |
| 17102614 | We recently found that human fibroblasts or endothelial cells with genetically-engineered reduction of proto-oncogene c-Myc expression switched with an increased frequency to a senescent state by a telomere-independent mechanism involving the polycomb group repressor Bmi-1 and the cyclin-dependent kinase inhibitor p16(INK4a) |
| 17026941 | The transcriptional inhibition of p16INK4a includes also the transcriptional repression by Bmi-1, and an epigenetic regulation which appears complex and remains incompletely understood |
| 17026941 | Furthermore, chromatin remodelling involving SWI/SNF complex, antagonist to Bmi-1, might activate INK4a expression |
| 17016587 | The expression of hTRAP and BMI-1 were detected by real-time PCR and Western blotting |
| 17016587 | The cell cycle-related genes, such as p16, p21, p53 and pRb, were not detected in F6 cells, while the expression of hTRAP and BMI-1 was significantly higher |
| 16936260 | Decreased expression of Bmi1 is closely associated with cellular senescence in small bile ducts in primary biliary cirrhosis |
| 16936260 | Bmi1 expression was examined immunohistochemically in livers taken from the patients with primary biliary cirrhosis (n=18) and other diseased (n=19) and normal livers (n=16) |
| 16936260 | Bmi1 was widely expressed in the nuclei of biliary epithelial cells in the control livers |
| 16911562 | To determine whether p16INK4A expression in human skin correlates with donor age, p16INK4A expression was analyzed by immunohistochemistry as well as the expression of the p16INK4A repressor BMI1 |
| 16911562 | BMI1 gene expression was significantly down-regulated with increasing donor age, whereas no striking age differences were observed for Ki67 |
| 16869752 | For example, the polycomb family proto-oncogene, Bmi-1, is consistently required for the self-renewal of diverse adult stem cells, as well as for the proliferation of cancer cells in the same tissues |
| 16869752 | Bmi-1 promotes stem cell self-renewal partly by repressing the expression of Ink4a and Arf, tumor suppressor genes that are commonly deleted in cancer |
| 16869752 | Despite ongoing Bmi-1 expression, Ink4a expression increases with age, potentially reducing stem cell frequency and function |
| 16537449 | Reduced c-Myc signaling triggers telomere-independent senescence by regulating Bmi-1 and p16(INK4a) |
| 16436134 | In the chymase cluster, a critical suppressor for cell senescence, BMI1 and the several related genes were found, suggesting that chymase expression may be closely related to cell senescence/quiescence events |
| 16319536 | This suggestion is in agreement with a growing body of evidence demonstrating that HSCs from Bmi-1(-/-) and ATM(-/-) mice can lose their ability to self-renew by undergoing premature senescence |
| 15958744 | Bmi1 loss produces an increase in astroglial cells and a decrease in neural stem cell population and proliferation |
| 15958744 | Loss of Bmi1 leads to a decreased brain size and causes progressive ataxia and epilepsy |
| 15958744 | Recently, Bmi1 was shown to control neural stem cell (NSC) renewal |
| 15958744 | However, the effect of Bmi1 loss on neural cell fate in vivo and the question whether the action of Bmi1 was intrinsic to the NSCs remained to be investigated |
| 15958744 | Here, we show that Bmi1 is expressed in the germinal zone in vivo and in NSCs as well as in progenitors proliferating in vitro, but not in differentiated cells |
| 15958744 | Loss of Bmi1 led to a decrease in proliferation in zones known to contain progenitors: the newborn cortex and the newborn and adult subventricular zone |
| 15958744 | This decrease was accentuated in vitro, where we observed a drastic reduction in NSC proliferation and renewal because of NSC-intrinsic effects of Bmi1 as shown by the means of RNA interference |
| 15958744 | Bmi1(-/-) mice also presented more astrocytes at birth, and a generalized gliosis at postnatal day 30 |
| 15958744 | At both stages, colocalization of bromodeoxyuridine and GFAP demonstrated that Bmi1 loss did not prevent astrocyte precursor proliferation |
| 15958744 | Supporting these observations, Bmi1(-/-) neurospheres generate preferentially astrocytes probably attributable to a different responsiveness to environmental factors |
| 15958744 | Bmi1 is therefore necessary for NSC renewal in a cell-intrinsic mode, whereas the altered cell pattern of the Bmi1(-/-) brain shows that in vivo astrocyte precursors can proliferate in the absence of Bmi1 |
| 15659210 | Senescence was accompanied by a decline in transcript levels of the polycomb gene Bmi-1, Ets1 and Ets2 transcription factors, and Id1, Id2 and Id3 helix-loop-helix proteins, suggesting roles for these genes in maintenance of cardiomyocyte proliferative capacity |
| 15647378 | The p16INK4a/RB braking pathway leading to senescence can be inhibited by introduction of Bmi-1, a polycomb-group gene, and human papillomavirus type 16 E7, but the extension of the life span of the UCBMSCs with hTERT did not require inhibition of the p16INK4a/RB pathway |
| 14722607 | Bmi1, stem cells, and senescence regulation |
| 14722607 | Bmi1 is required for the maintenance of adult stem cells in some tissues partly because it represses genes that induce cellular senescence and cell death |
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