Small interfering RNA-mediated α-enolase knockdown suppresses glycolysis and proliferation of human glioma U251 cells in vitro.
- Author:
Qi-Sheng LUO
1
,
2
;
Huang-de FU
;
Hai-Neng HUANG
;
Hua-Dong HUANG
;
Kun-Xiang LUO
;
Chuan-Yu LI
;
Cheng-Jian QIN
;
Xue-Yu LI
;
Hong-Cheng LUO
;
Jun-Li WANG
;
Qian-Li TANG
Author Information
- Publication Type:Journal Article
- From: Journal of Southern Medical University 2017;37(11):1484-1488
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of α-enolase (ENO1) in regulating glucose metabolism and cell growth in human glioma cells.
METHODSGlucose uptake and lactate generation were assessed to evaluate the changes in glucose metabolism in human glioma U251 cells with small interfering RNA (siRNA)-mediated ENO1 knockdown. MTT assay and 5-ethynyl-2'-deoxyuridine (EdU) staining were used to examine the cell growth and cell cycle changes following siRNA transfection of the cells.
RESULTSTransfection of U251 cells with siRNA-ENO1 markedly reduced glucose uptake (P=0.023) and lactate generation (P=0.007) in the cells and resulted in significant suppression of cell proliferation (*P<0.05) since the second day following the transfection. Transfection with siRNA-ENO1 also obviously suppressed cell cycle G1/S transition in the cells (P=0.0425). The expressions of HK2 and LDHA, the marker genes for glucose metabolism, were significantly down-regulated in the cells with siRNA-mediated ENO1 knockdown.
CONCLUSIONENO1 as a potential oncogene promotes glioma cell growth by positively modulating glucose metabolism.