miR-129-2 is frequently downregulated in multiple cancers. However, how it is silenced in cancers remainsunclear. 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 inGBM patient specimens and cultured cell lines. miR-129-2 expression could be restored upon treatment witha 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 Foxp1in GBMs. Consistently, expression of miR-129-2 significantly inhibits GBM cell proliferation in vitro. Theseresults 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.
(2015). Epigenetic Regulation of miR-129-2 Leads to Overexpression of PDGFRa and FoxP1 in Glioma Cells. Asian Pacific Journal of Cancer Prevention, 16(14), 6129-6133.
MLA
. "Epigenetic Regulation of miR-129-2 Leads to Overexpression of PDGFRa and FoxP1 in Glioma Cells". Asian Pacific Journal of Cancer Prevention, 16, 14, 2015, 6129-6133.
HARVARD
(2015). 'Epigenetic Regulation of miR-129-2 Leads to Overexpression of PDGFRa and FoxP1 in Glioma Cells', Asian Pacific Journal of Cancer Prevention, 16(14), pp. 6129-6133.
VANCOUVER
Epigenetic Regulation of miR-129-2 Leads to Overexpression of PDGFRa and FoxP1 in Glioma Cells. Asian Pacific Journal of Cancer Prevention, 2015; 16(14): 6129-6133.