miR-3189-targeted GLUT3 repression by HDAC2 knockdown inhibits glioblastoma tumorigenesis through regulating glucose metabolism and proliferation.

Sungmin KwakSeung-Ho ParkSung-Hak KimGi-Jun SungJi-Hye SongJi-Hoon JeongHyunhee KimChang Hoon HaSeong Who KimKyung-Chul Choi

Published in: Journal of experimental & clinical cancer research : CR (2022)

Our findings will demonstrate the central role of HDAC2 in GBM tumorigenesis through the reprogramming of glucose metabolism by controlling miR-3189-inhibited GLUT3 expression, providing a potential new therapeutic strategy for GBM treatment.

Keyphrases

long non coding rna
cell proliferation
poor prognosis
long noncoding rna
histone deacetylase
signaling pathway
cancer therapy
climate change
combination therapy