HCSGD entry for HMGA2


1. General information

Official gene symbolHMGA2
Entrez ID8091
Gene full namehigh mobility group AT-hook 2
Other gene symbolsBABL HMGI-C HMGIC LIPO STQTL9
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

color bar
This gene isn't in PPI subnetwork.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0000122Negative regulation of transcription from RNA polymerase II promoterIDAbiological_process
GO:0000228Nuclear chromosomeISScellular_component
GO:0000785ChromatinIEAcellular_component
GO:0000975Regulatory region DNA bindingIDAmolecular_function
GO:0000988Protein binding transcription factor activityIDAmolecular_function
GO:0001047Core promoter bindingIDAmolecular_function
GO:0001077RNA polymerase II core promoter proximal region sequence-specific DNA binding transcription factor activity involved in positive regulation of transcriptionIDAmolecular_function
GO:0001078RNA polymerase II core promoter proximal region sequence-specific DNA binding transcription factor activity involved in negative regulation of transcriptionIDAmolecular_function
GO:0001837Epithelial to mesenchymal transitionIMPbiological_process
GO:0002062Chondrocyte differentiationIDAbiological_process
GO:0003131Mesodermal-endodermal cell signalingIMPbiological_process
GO:0003677DNA bindingIEA NASmolecular_function
GO:0003680AT DNA bindingIDA IMPmolecular_function
GO:0003906DNA-(apurinic or apyrimidinic site) lyase activityIDAmolecular_function
GO:0004677DNA-dependent protein kinase activityIDAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005634NucleusIDA IEAcellular_component
GO:0006284Base-excision repairIDAbiological_process
GO:0006325Chromatin organizationTASbiological_process
GO:0006355Regulation of transcription, DNA-templatedIEA IMPbiological_process
GO:0006366Transcription from RNA polymerase II promoterIDAbiological_process
GO:0007067MitosisIEAbiological_process
GO:0007095Mitotic G2 DNA damage checkpointIDAbiological_process
GO:0007165Signal transductionIEAbiological_process
GO:0007275Multicellular organismal developmentTASbiological_process
GO:0007283SpermatogenesisIEAbiological_process
GO:0008134Transcription factor bindingIPImolecular_function
GO:0008301DNA binding, bendingIDA IMPmolecular_function
GO:0008584Male gonad developmentIEAbiological_process
GO:0009615Response to virusIEPbiological_process
GO:0010564Regulation of cell cycle processIDAbiological_process
GO:0010628Positive regulation of gene expressionIDAbiological_process
GO:0019899Enzyme bindingIEAmolecular_function
GO:0021846Cell proliferation in forebrainIEAbiological_process
GO:0021983Pituitary gland developmentIEAbiological_process
GO:0030261Chromosome condensationIEAbiological_process
GO:0030325Adrenal gland developmentIEAbiological_process
GO:0031052Chromosome breakageIDAbiological_process
GO:0031492Nucleosomal DNA bindingIDAmolecular_function
GO:0031507Heterochromatin assemblyIDAbiological_process
GO:0032993Protein-DNA complexIDAcellular_component
GO:0033144Negative regulation of intracellular steroid hormone receptor signaling pathwayIEAbiological_process
GO:0035019Somatic stem cell maintenanceIEAbiological_process
GO:0035497CAMP response element bindingIDAmolecular_function
GO:0035500MH2 domain bindingIDAmolecular_function
GO:0035501MH1 domain bindingIDAmolecular_function
GO:0035978Histone H2A-S139 phosphorylationIDAbiological_process
GO:0035985Senescence-associated heterochromatin focusIDAcellular_component
GO:0035986Senescence-associated heterochromatin focus assemblyIDAbiological_process
GO:0035987Endodermal cell differentiationIMPbiological_process
GO:0035988Chondrocyte proliferationIDAbiological_process
GO:0040018Positive regulation of multicellular organism growthIEAbiological_process
GO:0042769DNA damage response, detection of DNA damageIDAbiological_process
GO:0043065Positive regulation of apoptotic processIDAbiological_process
GO:0043066Negative regulation of apoptotic processIDAbiological_process
GO:0043392Negative regulation of DNA bindingIDAbiological_process
GO:0043922Negative regulation by host of viral transcriptionIDAbiological_process
GO:0045444Fat cell differentiationIMPbiological_process
GO:0045869Negative regulation of single stranded viral RNA replication via double stranded DNA intermediateIDAbiological_process
GO:0045892Negative regulation of transcription, DNA-templatedIDA IMPbiological_process
GO:0045893Positive regulation of transcription, DNA-templatedIDA IMPbiological_process
GO:0045944Positive regulation of transcription from RNA polymerase II promoterIDAbiological_process
GO:0046332SMAD bindingIPImolecular_function
GO:0046426Negative regulation of JAK-STAT cascadeIEAbiological_process
GO:0048333Mesodermal cell differentiationIMPbiological_process
GO:0048712Negative regulation of astrocyte differentiationIEAbiological_process
GO:0048762Mesenchymal cell differentiationIMPbiological_process
GO:0048863Stem cell differentiationIEPbiological_process
GO:0051091Positive regulation of sequence-specific DNA binding transcription factor activityIEAbiological_process
GO:00515755'-deoxyribose-5-phosphate lyase activityIDAmolecular_function
GO:0060123Regulation of growth hormone secretionIEAbiological_process
GO:0060613Fat pad developmentIEAbiological_process
GO:0070742C2H2 zinc finger domain bindingIMPmolecular_function
GO:0071141SMAD protein complexIDAcellular_component
GO:0071158Positive regulation of cell cycle arrestIDAbiological_process
GO:0090402Oncogene-induced cell senescenceIDAbiological_process
GO:2000036Regulation of stem cell maintenanceIMP TASbiological_process
GO:2000648Positive regulation of stem cell proliferationIDA IMPbiological_process
GO:2000679Positive regulation of transcription regulatory region DNA bindingIDAbiological_process
GO:2000685Positive regulation of cellular response to X-rayIDAbiological_process
GO:2000774Positive regulation of cellular senescenceIMPbiological_process
GO:2001022Positive regulation of response to DNA damage stimulusIDAbiological_process
GO:2001033Negative regulation of double-strand break repair via nonhomologous end joiningIDAbiological_process
GO:2001038Regulation of cellular response to drugIDAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.01977784660.85876965920.34129901901.0000000000

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Up0.5217231410
GSE13712_SHEARUp0.1740916917
GSE13712_STATICUp0.3572161285
GSE19018Up0.1698180230
GSE19899_A1Up0.3591288031
GSE19899_A2Up1.4586561518
PubMed_21979375_A1Down-0.0556555315
PubMed_21979375_A2Up0.3777266509
GSE35957Down-0.0386928238
GSE36640Down-0.8531382734
GSE54402Up0.9307005274
GSE9593Up0.1530563596
GSE43922--
GSE24585--
GSE37065--
GSE28863_A1Down-0.3201401700
GSE28863_A2Up0.3577376856
GSE28863_A3Down-0.3020132919
GSE28863_A4Up0.5410354716
GSE48662Down-0.3530659141

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-26a-5pMIMAT0000082MIRT000109Luciferase reporter assayFunctional MTI17563749
hsa-miR-125b-5pMIMAT0000423MIRT000348Luciferase reporter assayFunctional MTI17563749
hsa-miR-34a-5pMIMAT0000255MIRT000748MicroarrayFunctional MTI (Weak)19461653
hsa-let-7d-5pMIMAT0000065MIRT002005qRT-PCR//ChIP//Luciferase reporter assayFunctional MTI20395557
hsa-let-7d-5pMIMAT0000065MIRT002005Western blotFunctional MTI17957144
hsa-let-7e-5pMIMAT0000066MIRT002081Luciferase reporter assay//qRT-PCRFunctional MTI17437991
hsa-let-7b-5pMIMAT0000063MIRT002082Luciferase reporter assay//qRT-PCRFunctional MTI17437991
hsa-let-7g-5pMIMAT0000414MIRT002097Western blot//Reporter assayFunctional MTI18413726
hsa-let-7g-5pMIMAT0000414MIRT002097Luciferase reporter assayFunctional MTI17600087
hsa-let-7g-5pMIMAT0000414MIRT002097Luciferase reporter assayFunctional MTI18308936
hsa-let-7c-5pMIMAT0000064MIRT002322qRT-PCR//Western blot//Luciferase reporter assayFunctional MTI17600087
hsa-let-7c-5pMIMAT0000064MIRT002322Microarray//Northern blot//qRT-PCR//Western blotFunctional MTI17243163
hsa-let-7c-5pMIMAT0000064MIRT002322Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI18403645
hsa-let-7c-5pMIMAT0000064MIRT002322CLASHFunctional MTI (Weak)23622248
hsa-let-7a-5pMIMAT0000062MIRT002323qRT-PCR//Western blot//Luciferase reporter assayFunctional MTI17600087
hsa-let-7a-5pMIMAT0000062MIRT002323Luciferase reporter assayFunctional MTI18083101
hsa-let-7a-5pMIMAT0000062MIRT002323Luciferase reporter assayFunctional MTI17322030
hsa-let-7a-5pMIMAT0000062MIRT002323Luciferase reporter assayFunctional MTI18413822
hsa-let-7a-5pMIMAT0000062MIRT002323Luciferase reporter assay//Western blot//qRT-PCRFunctional MTI19179606
hsa-let-7a-5pMIMAT0000062MIRT002323CLASHFunctional MTI (Weak)23622248
hsa-miR-98-5pMIMAT0000096MIRT002999Northern blot//qRT-PCR//Western blot;OtherFunctional MTI17222355
hsa-miR-98-5pMIMAT0000096MIRT002999MicroarrayFunctional MTI (Weak)19088304
hsa-miR-370-3pMIMAT0000722MIRT003713Luciferase reporter assayNon-Functional MTI19179606
hsa-miR-185-5pMIMAT0000455MIRT004702Flow//Immunoblot//Microarray//qRT-PCRFunctional MTI (Weak)19688090
hsa-miR-760MIMAT0004957MIRT036768CLASHFunctional MTI (Weak)23622248
hsa-let-7f-5pMIMAT0000067MIRT051403CLASHFunctional 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-let-7b-5pMIMAT00000631hsa-let-7b{Western blot}{Western blot}{overexpression by siRNA transfection}{underexpression by 2'-O-Me antisense miRNA oligonucleotides}17437991
hsa-let-7b-5pMIMAT00000634hsa-let-7b{Western blot}{Western blot}{overexpression by siRNA transfection}{underexpression by 2'-O-Me antisense miRNA oligonucleotides}17437991
hsa-let-7b-5pMIMAT00000635hsa-let-7b{Western blot}{Western blot}{overexpression by siRNA transfection}{underexpression by 2'-O-Me antisense miRNA oligonucleotides}17437991
hsa-let-7b-5pMIMAT00000632hsa-let-7b{Western blot}{Western blot}{overexpression by siRNA transfection}{underexpression by 2'-O-Me antisense miRNA oligonucleotides}17437991
hsa-let-7b-5pMIMAT00000633hsa-let-7b{Western blot}{Western blot}{overexpression by siRNA transfection}{underexpression by 2'-O-Me antisense miRNA oligonucleotides}17437991
hsa-let-7b-5pMIMAT00000636hsa-let-7b{Western blot}{Western blot}{overexpression by siRNA transfection}{underexpression by 2'-O-Me antisense miRNA oligonucleotides}17437991
hsa-let-7e-5pMIMAT00000663hsa-let-7e{Western blot}{Western blot}{overexpression by siRNA transfection}{underexpression by 2'-O-Me antisense miRNA oligonucleotides}17437991
hsa-let-7e-5pMIMAT00000666hsa-let-7e{Western blot}{Western blot}{overexpression by siRNA transfection}{underexpression by 2'-O-Me antisense miRNA oligonucleotides}17437991
hsa-let-7e-5pMIMAT00000664hsa-let-7e{Western blot}{Western blot}{overexpression by siRNA transfection}{underexpression by 2'-O-Me antisense miRNA oligonucleotides}17437991
hsa-let-7e-5pMIMAT00000662hsa-let-7e{Western blot}{Western blot}{overexpression by siRNA transfection}{underexpression by 2'-O-Me antisense miRNA oligonucleotides}17437991
hsa-let-7e-5pMIMAT00000661hsa-let-7e{Western blot}{Western blot}{overexpression by siRNA transfection}{underexpression by 2'-O-Me antisense miRNA oligonucleotides}17437991
hsa-let-7e-5pMIMAT00000665hsa-let-7e{Western blot}{Western blot}{overexpression by siRNA transfection}{underexpression by 2'-O-Me antisense miRNA oligonucleotides}17437991
hsa-let-7a-5pMIMAT00000622hsa-let-7a{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17600087
hsa-let-7a-5pMIMAT00000623hsa-let-7a{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17600087
hsa-let-7a-5pMIMAT00000625hsa-let-7a{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17600087
hsa-let-7a-5pMIMAT00000627hsa-let-7a{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17600087
hsa-let-7a-5pMIMAT00000621hsa-let-7a{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17600087
hsa-let-7a-5pMIMAT00000624hsa-let-7a{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17600087
hsa-let-7a-5pMIMAT00000626hsa-let-7a{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17600087
hsa-let-7g-5pMIMAT00004141hsa-let-7g{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17600087
hsa-let-7g-5pMIMAT00004143hsa-let-7g{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17600087
hsa-let-7g-5pMIMAT00004145hsa-let-7g{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17600087
hsa-let-7g-5pMIMAT00004144hsa-let-7g{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17600087
hsa-let-7g-5pMIMAT00004147hsa-let-7g{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17600087
hsa-let-7g-5pMIMAT00004146hsa-let-7g{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17600087
hsa-let-7g-5pMIMAT00004142hsa-let-7g{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17600087
hsa-miR-98-5pMIMAT00000965hsa-miR-98{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17222355
hsa-miR-98-5pMIMAT00000962hsa-miR-98{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17222355
hsa-miR-98-5pMIMAT00000964hsa-miR-98{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17222355
hsa-miR-98-5pMIMAT00000966hsa-miR-98{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17222355
hsa-miR-98-5pMIMAT00000967hsa-miR-98{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17222355
hsa-miR-98-5pMIMAT00000963hsa-miR-98{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17222355
hsa-miR-98-5pMIMAT00000961hsa-miR-98{Western blot}{Western blot}{overexpression by miRNA precursor transfection}{underexpression by anti-miRNA oligonucleotides}17222355
hsa-miR-204-5pMIMAT0000265NAhsa-miR-20420369013
hsa-miR-185-5pMIMAT0000455NAhsa-miR-18519688090
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6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 15 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

24476133Moreover, induction of SIPS was mediated by HMGA2, which colocalized to senescence-associated heterochromatin foci
23969248Rb protein is essential to the senescence-associated heterochromatic foci formation induced by HMGA2 in primary WI38 cells
23969248Surprisingly, although high mobility group A2 protein (HMGA2) can promote tumorigenesis and inhibit Rb function in tumor cells, high-level expression of HMGA2 is sufficient to induce SAHF formation in primary cells
23969248In this study, we established the cellular senescence and SAHF assembly WI38 cell model by ectopic expression of HMGA2, in which typical senescent markers were seen, including notable upregulation of p53, p21 and p16, and elevated SA-beta-galactosidase staining together with downregulation of E2F target genes
23969248We then showed that the Rb pathway inhibitor E7 protein was able to partly abolish the ability of SAHF formation after HMGA2 expression in WI38 cells, indicating that Rb is a crucial factor for HMGA2-induced SAHF formation
23969248However, Rb depletion did not completely rescue the cell growth arrest induced by HMGA2, suggesting that Rb is not an exclusive pathway for HMGA2-induced senescence in WI38 cells
23881689HMGA2 expression in white adipose tissue linking cellular senescence with diabetes
23881689The molecular mechanism of the gain of adipose tissue is linked with the expression of high mobility group protein AT-hook 2 (HMGA2), and recent studies revealed an association with a SNP near HMGA2
23881689We found a significant higher HMGA2 expression in obese individuals than in non-obese patients
23881689Furthermore, the HMGA2 expression in white adipose tissue in patient with type 2 diabetes was significantly higher than in nondiabetic patients
23881689There is an association between the DNA-binding nonhistone protein HMGA2 and the risk of developing T2D that remains mechanistically unexplained so far
23276696HMGA2 regulates the in vitro aging and proliferation of human umbilical cord blood-derived stromal cells through the mTOR/p70S6K signaling pathway
23276696The human high-mobility group protein A2 (HMGA2) protein is an architectural transcription factor that transforms chromatin structure by binding to DNA
23276696Recently, it has been reported that HMGA2 is highly expressed in fetal neural stem cells and has the capacity to promote stemness
23276696In the present study, we evaluated the direct effects of HMGA2 on the cellular aging and proliferation of hUCBSCs and investigated potential regulatory mechanisms responsible for the corresponding functions
23276696We found that the overexpression of HMGA2 enhanced proliferation and reduced or even reversed the in vitro aging process of hUCBSCs
23276696Furthermore, HMGA2 inhibition compromised cell proliferation and adipogenic differentiation in early-stage hUCBSCs
23276696These results provide novel insights into the mechanism by which HMGA2 regulates the in vitro aging and proliferation of hUCBSCs
23072816We identified 2 microRNAs, microRNA-10A* (miR-10A*), and miR-21, and their common target gene Hmga2 as critical regulators for EPC senescence
23072816Overexpression of miR-10A* and miR-21 in young EPCs suppressed Hmga2 expression, caused EPC senescence, as evidenced by senescence-associated beta-galactosidase upregulation, decreased self-renewal potential, increased p16(Ink4a)/p19(Arf) expression, and resulted in impaired EPC angiogenesis in vitro and in vivo, resembling EPCs derived from aged mice
23072816In contrast, suppression of miR-10A* and miR-21 in aged EPCs increased Hmga2 expression, rejuvenated EPCs, resulting in decreased senescence-associated beta-galactosidase expression, increased self-renewal potential, decreased p16(Ink4a)/p19(Arf) expression, and improved EPC angiogenesis in vitro and in vivo
23072816Importantly, these phenotypic changes were rescued by miRNA-resistant Hmga2 cDNA overexpression
23072816CONCLUSIONS: miR-10A* and miR-21 regulate EPC senescence via suppressing Hmga2 expression and modulation of microRNAs may represent a potential therapeutic intervention in improving EPC-mediated angiogenesis and vascular repair
21515304Increase in senescent associated markers such as p21, HMGA2 and PAI-1 was more prominent in DPV treated cells compared to similar dose of H(2)O(2)
21498692HMGA2 and p14Arf: major roles in cellular senescence of fibroids and therapeutic implications
21498692RESULTS: In fibroid cells, expression of HMGA2 decreased with passaging while that of p14(Arf) increased
21498692CONCLUSION: p14(Arf) and HMGA2 seem to play a pivotal role in controlling the growth of fibroid cells
21456046HMGA2 is a major regulator of benign tumorigenesis from mesenchyme-derived tissues and stem-cell self-renewal
21456046To repress the oncogenic activity of HMGA2, the lin-28-let-7 axis is thought to increasingly repress the expression of HMGA2 with age
21456046The expression of both genes was inversely correlated during senescence in vitro but contrary to the expectations in adipose tissue derived stem cells (ADSCs) stimulation of HMGA2 by FGF1 increased the expression of p14(Arf)
21456046Based on the assumption that in ADSCs p14(Arf) is repressing HMGA2, siRNA silencing of p14(Arf) was performed resulting in a significant upregulation of HMGA2
21456046To see if p14(Arf) can repress HMGA2 by a TP53-dependent mechanism, nutlin-3, a known MDM2 antagonist, was used which not only increased the activity of the senescence, associated markers p21 and beta-galactosidase, but also decreased the expression of HMGA2, suggesting that p14(Arf) indeed influences HMGA2 by a p53-dependent mechanism because nutlin-3 stabilizes p53
21456046Accordingly, the HMGA2 response triggered by serum was reduced by treatment of ADSCs with nutlin-3
21456046As to the interaction between HMGA2 and p14(Arf) in benign tumorigenesis, we propose a model where akin to MSC self-renewal during tissue repair the simultaneous increase of p14(Arf) with HMGA2 ensures genomic stability, whereas in turn p14(Arf) can repress HMGA2 via TP53
20652617Here, we observed that the cellular senescence of human umbilical cord blood-derived multipotent stem cells (hUCB-MSCs) caused by inhibition of histone deacetylase (HDAC) activity leads to down-regulation of high mobility group A2 (HMGA2) and, on the contrary, to up-regulation of p16(INK)(4)(A), p21(CIP)(1)(/WAF)(1) and p27(KIP)(1)
20652617We confirmed that miR-23a, miR-26a and miR-30a inhibit HMGA2 to accelerate the progress of senescence
20652617These findings suggest that HDACs may play important roles in cellular senescence by regulating the expression of miRNAs that target HMGA2 through histone modification
19217096MAIN OUTCOME MEASURE(S): Senescence measured by percentage of SA-beta-Gal-positive cells; levels of let-7 microRNAs measured by RT-PCR and MISH; expression of p16(INK4a), Ki-67, HMGA1, and HMGA2 scaled by immunoreactivity
19070572HMGA2, microRNAs, and stem cell aging
18983959Ink4a/Arf regulation by let-7b and Hmga2: a genetic pathway governing stem cell aging
18983959In a recent issue of Cell, Nishino and colleagues (2008) show that Hmga2 maintains neural stem cell (NSC) function in young mice through repression of the Ink4a/Arf locus; in contrast, during aging, elevated let-7b blocks Hmga2 and contributes to declining NSC function
18505920HMGA2 participates in transformation in human lung cancer
18505920Although previous studies have established a prominent role for HMGA1 (formerly HMG-I/Y) in aggressive human cancers, the role of HMGA2 (formerly HMGI-C) in malignant transformation has not been clearly defined
18505920The HMGA gene family includes HMGA1, which encodes the HMGA1a and HMGA1b protein isoforms, and HMGA2, which encodes HMGA2
18505920HMGA1 proteins also appear to participate in cell cycle regulation and malignant transformation, whereas HMGA2 has been implicated primarily in the pathogenesis of benign, mesenchymal tumors
18505920Here, we show that overexpression of HMGA2 leads to a transformed phenotype in cultured lung cells derived from normal tissue
18505920Conversely, inhibiting HMGA2 expression blocks the transformed phenotype in metastatic human non-small cell lung cancer cells
18505920Moreover, we show that HMGA2 mRNA and protein are overexpressed in primary human lung cancers compared with normal tissue or indolent tumors
18505920In addition, there is a statistically significant correlation between HMGA2 protein staining by immunohistochemical analysis and tumor grade (P < 0
18505920Our results indicate that HMGA2 is an oncogene important in the pathogenesis of human lung cancer
18505920Although additional studies with animal models are needed, these findings suggest that targeting HMGA2 could be therapeutically beneficial in lung cancer and other cancers characterized by increased HMGA2 expression
17158953However, the simultaneous ectopic expression of hemagglutinin-tagged HMGA2 and N-terminally EGFP-tagged histone H1 leads to significant SAHF formation (P < 0
16901784These antiproliferative activities are canceled by coexpression of the HDM2 and CDK4 oncogenes, which are often coamplified with HMGA2 in human cancers
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