Glut-1, HK-II, and PCNA expression are related to uptake of 18F-FDG uptake in lung cancer

HK2 functions as a novel oncogene in lung cancer and may be a potential therapeutic target for lung cancer.

HK2modulated glucose metabolism was significantly upregulated by overexpression of miR155. Notably, inhibition of miR155 sensitized lung cancer cells to irradiation via suppression of glucose metabolism.

AKT inhibition blocks miR-124 silencing-induced AKT1/2, glucose transporter 1, hexokinase II activation, cell proliferation, and glycolytic or energy metabolism changes. In summary, this study demonstrated that miR-124 is able to inhibit proliferation, glycolysis, and energy metabolism, potentially by targeting AKT1/2-glucose transporter 1/hexokinase II in non-small cell lung cancer cells.

the results indicated that JB inhibits glycolysis by down-regulating HK2 expression through inactivating the Akt/mTOR pathway in non-small cell lung cancer (NSCLC) cells, suggesting that JB might be a potential therapeutic agent for the treatment of NSCLC.

miR-206 regulates non-small-cell lung cancer cell aerobic glycolysis by targeting hexokinase 2.