HCSGD entry for PTTG1
1. General information
| Official gene symbol | PTTG1 |
|---|---|
| Entrez ID | 9232 |
| Gene full name | pituitary tumor-transforming 1 |
| Other gene symbols | EAP1 HPTTG PTTG TUTR1 |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000278 | Mitotic cell cycle | TAS | biological_process |
| GO:0003700 | Sequence-specific DNA binding transcription factor activity | TAS | molecular_function |
| GO:0004869 | Cysteine-type endopeptidase inhibitor activity | NAS | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005634 | Nucleus | IDA IEA | cellular_component |
| GO:0005737 | Cytoplasm | IDA IEA | cellular_component |
| GO:0005829 | Cytosol | TAS | cellular_component |
| GO:0006259 | DNA metabolic process | IEA | biological_process |
| GO:0006281 | DNA repair | IEA | biological_process |
| GO:0006355 | Regulation of transcription, DNA-templated | TAS | biological_process |
| GO:0006366 | Transcription from RNA polymerase II promoter | TAS | biological_process |
| GO:0007059 | Chromosome segregation | IEA | biological_process |
| GO:0007067 | Mitosis | IEA | biological_process |
| GO:0007283 | Spermatogenesis | TAS | biological_process |
| GO:0010466 | Negative regulation of peptidase activity | NAS | biological_process |
| GO:0010951 | Negative regulation of endopeptidase activity | NAS | biological_process |
| GO:0017124 | SH3 domain binding | IEA | molecular_function |
| GO:0031145 | Anaphase-promoting complex-dependent proteasomal ubiquitin-dependent protein catabolic process | TAS | biological_process |
| GO:0043086 | Negative regulation of catalytic activity | NAS | biological_process |
| GO:0050790 | Regulation of catalytic activity | NAS | biological_process |
| GO:0051276 | Chromosome organization | IEA | biological_process |
| GO:0052547 | Regulation of peptidase activity | NAS | biological_process |
| GO:0052548 | Regulation of endopeptidase activity | NAS | biological_process |
| GO:2001141 | Regulation of RNA biosynthetic process | TAS | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.8774381672 | 0.0000136659 | 0.9999902473 | 0.0071627451 |
- 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 | Down | -2.6007047938 |
| GSE13712_SHEAR | Down | -0.1497852368 |
| GSE13712_STATIC | Down | -0.3498530052 |
| GSE19018 | Up | 1.0589401154 |
| GSE19899_A1 | Down | -3.8800452764 |
| GSE19899_A2 | Down | -3.2022110339 |
| PubMed_21979375_A1 | Down | -3.8108605519 |
| PubMed_21979375_A2 | Down | -4.1770625798 |
| GSE35957 | Down | -4.5134619222 |
| GSE36640 | Down | -3.7725212059 |
| GSE54402 | Down | -0.9805418022 |
| GSE9593 | Down | -1.9527728046 |
| GSE43922 | Down | -1.7714856041 |
| GSE24585 | Down | -0.1193628484 |
| GSE37065 | Down | -0.1361911657 |
| GSE28863_A1 | Down | -0.0462724646 |
| GSE28863_A2 | Up | 0.3636219736 |
| GSE28863_A3 | Up | 0.2186431170 |
| GSE28863_A4 | Up | 0.1515602044 |
| GSE48662 | Down | -2.3656091231 |
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-423-5p | MIMAT0004748 | MIRT038103 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-320a | MIMAT0000510 | MIRT044427 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-186-5p | MIMAT0000456 | MIRT044923 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-26a-5p | MIMAT0000082 | MIRT050118 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-17-5p | MIMAT0000070 | MIRT050987 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-let-7b-5p | MIMAT0000063 | MIRT052149 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
No target information from mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 11 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 25627474 | BACKGROUND: Pituitary tumor-transforming gene-1 (PTTG1) is a transcription factor that can affect transcriptional activity, angiogenesis, and cell senescence |
| 25627474 | We examined PTTG1 mRNA and protein expression in gastric cancer (GC) cell lines and tissues to determine its value as a biomarker for GC diagnosis and therapy |
| 25627474 | METHODS: PTTG1 mRNA expression from 78 GC cases and paired adjacent normal mucosa (PCR cohort) as well as from five gastric cell lines was assessed using qRT-PCR |
| 25627474 | PTTG1 protein expression from 98 GC cases, their paired adjacent normal mucosa, and 23 gastric intraepithelial neoplasia (GIN) cases was examined using immunohistochemistry (IHC cohort) |
| 25627474 | The correlation between PTTG1 mRNA and protein expression and GC clinicopathological parameters was analyzed |
| 25627474 | RESULTS: PTTG1 mRNA expression in GC tissues and cell lines was significantly increased compared with adjacent normal gastric mucosa and normal gastric mucous cell lines (p < 0 |
| 25627474 | PTTG1 expression was nuclear and cytoplasmic, with higher cytoplasmic expression |
| 25627474 | PTTG1 immunostaining significantly differed in GC (95 |
| 25627474 | Multivariate Cox regression analysis revealed that PTTG1 mRNA and protein expression are independent prognostic factors for GC patient survival |
| 25627474 | CONCLUSION: Our results suggest that PTTG1 is a promising target for GC diagnosis and therapy |
| 24853433 | Our previous studies have shown that radiation induces senescence of human breast cancer cells that display low expression of securin, a protein involved in control of the metaphase-anaphase transition and anaphase onset |
| 24816985 | Changes in PTTG1 by human TERT gene expression modulate the self-renewal of placenta-derived mesenchymal stem cells |
| 24816985 | The objectives of this study were to generate immortalized MSCs derived from MSCs isolated from placenta (naive) by human TERT gene transfection with the AMAXA gene delivery system, to compare their characteristics, and to investigate whether increased TERT expression affected the pituitary tumor transforming gene (PTTG1; also known as securin), which is involved in chromosome segregation during mitosis |
| 24816985 | TERT-immortalized cells (TERT+) with a prolonged life span displayed high PTTG1 expression |
| 24816985 | TERT+ cells also retained the stemness capacity and multipotency of naive cells and displayed high PTTG1 expression |
| 24816985 | However, down-regulation of PTTG1 by treatment with short interfering RNA induced cell senescence and decreased telomerase activity |
| 24816985 | Moreover, TERT bound to PTTG1 formed complexes with chaperones such as Ku70 and heat shock protein 90 |
| 24816985 | Thus, placental MSCs immortalized by TERT gene transfection display differentiation potential and exhibit enhanced self-renewal through a balanced interaction of PTTG1 and chaperones |
| 24816985 | The interaction between TERT and PTTG1 by association of Ku70 might be important for the enhancement of the limited self-renewal activity of MSCs and for understanding the regulatory mechanisms of self-renewal |
| 23591770 | Securin overexpression correlates with poor prognosis in various tumours |
| 23591770 | We have previously shown that securin depletion promotes radiation-induced senescence and enhances radiosensitivity in human cancer cells |
| 22789011 | INTRODUCTION: hPTTG1 (human pituitary tumor-transforming gene 1) is an oncogene overexpressed in breast cancer and several other types of cancer |
| 22789011 | Increased hPTTG1 expression has been shown to be associated with poor patient outcomes in breast cancer |
| 22789011 | Although hPTTG1 overexpression plays important roles in promoting the proliferation, invasion, and metastasis of cancer cells, it also has been suggested to induce cellular senescence |
| 22789011 | Deciphering the mechanism by which hPTTG1 overexpression induces these contradictory actions in breast cancer cells is critical to our understanding of the role of hPTTG1 in breast cancer development |
| 22789011 | The interplay between hPTTG1 overexpression and chemokine C-X-C motif receptor 2 (CXCR2)/p21-dependent senescence in tumor growth and metastasis of MCF-7 cells was investigated by orthotopic transplantation of severe combined immunodeficiency (SCID) mice |
| 22789011 | Herein, we showed that hPTTG1 overexpression reinforced senescence through the CXCR2/p21 signaling |
| 22789011 | Furthermore, hPTTG1 overexpression activated NF-kappaB signaling to transactivate the expression of interleukin (IL)-8 and growth-regulated oncogene alpha (GROalpha) to execute CXCR2 signaling in MCF-7 cells |
| 22789011 | Our in vitro and in vivo results demonstrated that hPTTG1 overexpression reinforces senescence through CXCR2 signaling, and the evasion of CXCR2/p21-dependent senescence was critical to hPTTG1 exerting its oncogenic potential |
| 22789011 | CONCLUSIONS: Our findings provide novel molecular insights into hPTTG1-induced senescence and identify a novel mechanism by which hPTTG1 promotes metastasis by regulating the senescence-associated microenvironment |
| 21858218 | PTTG1 attenuates drug-induced cellular senescence |
| 21858218 | As PTTG1 (pituitary tumor transforming gene) abundance correlates with adverse outcomes in cancer treatment, we determined mechanisms underlying this observation by assessing the role of PTTG1 in regulating cell response to anti-neoplastic drugs |
| 21858218 | HCT116 cells devoid of PTTG1 (PTTG1(-/-)) exhibited enhanced drug sensitivity as assessed by measuring BrdU incorporation in vitro |
| 21858218 | PTTG1 also regulated SW620 colon cancer cells response to doxorubicin and TSA mediated by p21 |
| 21858218 | PTTG1(-/-) tumor tissue derived from excised tumors exhibited increased doxorubicin-induced senescence |
| 21858218 | As senescence is a determinant of cell responses to anti-neoplastic treatments, these findings suggest PTTG1 as a tumor cell marker to predict anti-neoplastic treatment outcomes |
| 21536883 | Here, we generated germline transgenic zebrafish with overexpression of pituitary tumor transforming gene (PTTG/securin) targeted to the adenohypophyseal proopiomelanocortin (POMC) lineage, which recapitulated early features pathognomonic of corticotroph adenomas, including corticotroph expansion and partial glucocorticoid resistance |
| 20457353 | Depletion of securin induces senescence after irradiation and enhances radiosensitivity in human cancer cells regardless of functional p53 expression |
| 20457353 | This study investigated the role of securin in radiation-induced apoptosis and senescence in human cancer cells |
| 20457353 | Securin gene knockdown was performed by small interfering RNA and small hairpin RNA in HCT116 and MDA-MB-231 cells, respectively |
| 20457353 | RESULTS: Radiation was found to induce apoptosis in securin wild type HCT116 cells but induced senescence in securin-null cells |
| 20457353 | Restoration of securin reduced senescence and increased cell survival in securin-null HCT116 cells after irradiation |
| 20457353 | Securin gene knockdown switches irradiation-induced apoptosis to senescence in both HCT116 p53-null and MDA-MB-231 cells |
| 20457353 | CONCLUSIONS: Our results demonstrated that the level of securin expression plays a determining role in the radiosensitivity and fate of cells |
| 20457353 | Depletion of securin impairs DNA repair after irradiation, increasing DNA damage and promoting senescence in the residual surviving cells regardless of functional p53 expression |
| 20457353 | The knockdown of securin may contribute to a novel radiotherapy protocol for the treatment of human cancer cells that are resistant to irradiation |
| 20153804 | Pituitary senescence: the evolving role of Pttg |
| 20153804 | Both deletion and over-expression of pituitary tumor transforming gene (Pttg) promote chromosomal instability and aneuploidy |
| 20153804 | Pttg deletion abrogates tumor development by activating p53/p21-dependent senescence pathways |
| 20153804 | Abundant PTTG in GH-secreting pituitary adenomas also triggers p21-dependent senescence |
| 19433493 | Pituitary tumor-transforming gene-1 (PTTG1) is a transforming gene first discovered in rat pituitary tumor cells |
| 19433493 | It possesses transcriptional activity and also has securin functions |
| 19433493 | PTTG1 has several validated transcriptional targets that are involved in different cellular processes |
| 19433493 | PTTG1 activates c-Myc in NIH 3T3 cells, suggesting a role in cell transformation |
| 19433493 | PTTG1 induces fibroblast growth factor 2 expression and promotes tumor angiogenesis |
| 19433493 | PTTG1 activates cyclin D3 and represses p21 expression, indicating a role in cell cycle regulation and cell senescence |
| 19433493 | Here, we review PTTG1 transcriptional targets and their functions |
| 19213844 | Pituitary tumor transforming gene (PTTG) encodes a securin protein critical in regulating chromosome separation |
| 19213844 | PTTG-null (PTTG(-/-)) mice exhibit pancreatic beta-cell hypoplasia and insulinopenic diabetes |
| 19213844 | We tested whether PTTG deletion causes beta-cell senescence, resulting in diminished beta-cell mass |
| 19213844 | We examined beta-cell mass, proliferation, apoptosis, neogenesis, cell size, and senescence in PTTG(-/-) and WT mice from embryo to young adulthood before diabetes is evident |
| 19213844 | The roles of cyclin-dependent kinase inhibitors and DNA damage in the pathogenesis of diabetes in PTTG(-/-) mice were also addressed |
| 19213844 | Relative beta-cell mass in PTTG(-/-) mice began to decrease at 2-3 wk, whereas beta-cell proliferation rate was initially normal but decreased in PTTG(-/-) mice beginning at 2 months |
| 19213844 | Apoptosis was also much more evident in PTTG(-/-) mice |
| 19213844 | At 1 month, beta-cell neogenesis was robust in wild-type mice but was absent in PTTG(-/-) mice |
| 19213844 | In addition, the size of beta-cells became larger and macronuclei were prominent in PTTG(-/-) animals |
| 19213844 | Cyclin-dependent kinase inhibitor p21 was progressively up-regulated in PTTG(-/-) islets, and p21 deletion partially rescued PTTG(-/-) mice from development of diabetes |
| 19213844 | We conclude that beta-cell apoptosis and senescence contribute to the diminished beta-cell mass in PTTG(-/-) mice, likely secondary to DNA damage |
| 19213844 | Our results also suggest that ductal progenitor beta-cells are exhausted by excessive neogenesis induced by apoptosis in PTTG(-/-) mice |
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