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STAT6 is epigenetically down-regulated in glioma and regulates cell viability

Authors
Park, Soo Jung; Jou, Ilo
Department
Department of Pharmacology, Ajou University School of Medicine
Abstract
DNA hypermethylation-induced silencing of tumor suppressor is a well-recognized mechanism of epigenetic modification which occurs human tumors. In this study, we demonstrated that the transcription factor STAT6 was markedly down-regulated in glioma tissues and glioma stem cells, comparing to non-tumor neighboring tissues. We also found that CpG islands in STAT6 promoter are hypermethylated in both glioma tissues and glioma stem cells. These findings led us to hypothesize that STAT6 may act as tumor suppressor in glioma. We examined it by overexpressing STAT6 in U373MG or glioma stem cells (where STAT6 is scarcely expressed) or down-regulating STAT6 in U87MG (where STAT6 is highly expressed). STAT6 overexpression decreased cell viability, whereas its down-regulation increased it, especially under hypoxic conditions which mimic tumor microenvironments. Furthermore, protein levels of HIF-1, the major transcription factor mediating hypoxic adaptation and survival, is decreased in STAT6-overexpressing cells but increased in STAT6-knockdown cells. This result indicates that the effects of STAT6 on hypoxic cell viability are mediated via regulation of HIF-1 expression. Interestingly, in glioma stem cells, STAT6 overexpression was found to down-regulate the exression of stemness markers including NANOG, NESTIN and OLIOG2. Taken together, these results suggest that STAT6 acts as a negative regulator of HIF-1 and stemness in glioma, providing further evidence for its potential as a tumor suppressor.
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