Epigenetic regulation of miR-129-2 leads to overexpression of PDGFRa and FoxP1 in glioma cells

Xiang Yang Tian, Ling Zhang, Lai Guang Sun, Ming Li

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


miR-129-2 is frequently downregulated in multiple cancers. However, how it is silenced in cancers remains unclear. Here we investigated the expression profile and potential biological function of miR-129-2 in glioblastoma (GBM), the most common and lethal form of brain tumors in adults. We showed that miR-129-2 is lost in GBM patient specimens and cultured cell lines. miR-129-2 expression could be restored upon treatment with a histone deadetylase inhibitor (trichostatin A) but not a DNA methylation inhibitor (5-Aza-2'-deoxycytidine), and more profound effect was observed with the treatment of these two drugs in combination. Furthermore, forced expression of miR-129-2 repressed the expression of major oncogenic genes such as PDGFRa and Foxp1 in GBMs. Consistently, expression of miR-129-2 significantly inhibits GBM cell proliferation in vitro. These results reveal that miR-129-2 is epigenetically regulated and functions as a tumor suppressor gene in GBMs, suggesting it may serve as a potential therapeutic target for GBM treatment.

Original languageEnglish (US)
Pages (from-to)6129-6133
Number of pages5
JournalAsian Pacific Journal of Cancer Prevention
Issue number14
StatePublished - 2015
Externally publishedYes


  • Epigenetic regulation
  • Glioblastoma
  • MicroRNA-129


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