OBJECTIVE: To investigate the role of α-enolase (ENO1) in regulating glucose metabolism and cell growth in human glioma cells. METHODS: Glucose 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. RESULTS: Transfection 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. CONCLUSION: ENO1 as a potential oncogene promotes glioma cell growth by positively modulating glucose metabolism.
OBJECTIVE: To investigate the role of α-enolase (ENO1) in regulating glucose metabolism and cell growth in humanglioma cells. METHODS:Glucose uptake and lactate generation were assessed to evaluate the changes in glucose metabolism in humanglioma 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. RESULTS: Transfection 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. CONCLUSION:ENO1 as a potential oncogene promotes glioma cell growth by positively modulating glucose metabolism.
Authors: Nzinga Mack; Elizabeth A Mazzio; David Bauer; Hernan Flores-Rozas; Karam F A Soliman Journal: Anticancer Res Date: 2017-03 Impact factor: 2.480
Authors: Hajnalka Harami-Papp; Lőrinc S Pongor; Gyöngyi Munkácsy; Gergő Horváth; Ádám M Nagy; Attila Ambrus; Péter Hauser; András Szabó; László Tretter; Balázs Győrffy Journal: Oncotarget Date: 2016-10-11
Authors: S Oudard; F Arvelo; L Miccoli; F Apiou; A M Dutrillaux; M Poisson; B Dutrillaux; M F Poupon Journal: Br J Cancer Date: 1996-09 Impact factor: 7.640