Objective      To determine the effect of homo sapiensv-Ki-ras2 Kirsten rat sarcoma viral oncogenes homologue (KRAS) on the glycolysis in lung cancer cells and investigate the underlying possible mechanism.       Methods      The expression of KRAS

hexokinase 2 (HK2)

and pyruvate kinase M2 (PKM2) in 3 lung cancer cell lines H1299

A549 and SPC-A was determined with real-time PCR and Western blotting. Lactate concentration was assessed in 48 hours’ culture. After H1299 cells were transfected with negative control and KRAS-shRNA respectively

the expression of the 3 molecules was assessed with real-time PCR and Western blot analysis. After treatment with TNF- alpha in the negative control and H1299-KRAS-shRNA cells

the expression levels of HK2 and PKM2

as well as the lactate concentration were assessed.       Results      The expression of KRAS

HK2 and PKM2 as well as the lactate secretion in H1299 cells were the highest among above 3 lung cancer cell lines. Compared to the negative control group

lentiviral shRNA interference significantly inhibited KRAS expression at mRNA and protein levels (P0.05). Moreover

the mRNA and protein levels of HK2 and PKM2 were also decreased in KRAS-shRNA transfected H1299 cells

compared with negative control (P0.05). TNF-α enhanced KRAS

HK2 and PKM2 in both the negative control and H1299-KRAS-shRNA cells (P0.05). In addition

KRAS-shRNA significantly decreased TNF-α elevated lactate concentrations in the supernatant compared with the negative control (P0.05).       Conclusion       KRAS promotes the glycolysis in lung cancer cells via modulating glycolysis related enzymes.