Molecular Mechanisms of the Gastric Cancer Cells Resisting Anoikis

Objective To explore the mechanisms of signal transduction by which gastric cancer cells resist anoikis. Methods Soft agar assay was used to observe the effect of the specific signal molecular inhibitors on the anchorage-independent growth of the gastric cancer cells. Flow cytometry ( FCM) was employed to examine the cell cycles and apoptotic rate of the gastric cancer cells cultured in suspension with the signal molecular inhibitors. Western blot analysis was performed to study the expression level and activation of some important signal molecules of the detached gastric cancer cells. Results Signal molecular inhibitors, Genistein, AG17 and AG825 completely inhibited the cell clone formation, arrested the gastric cancer cells in different cell cycles and induced cell anoikis significantly. But when cells were treated with LY, PD and SB, its clone size was smaller and the clones were less as compared with that of control. The treatment induced anoikis to a small extent, but arrested cells at various cell cycles. Western blot revealed that, 24 hours after detachment of gastric cancer cells, phosphorylation level of protein tyrosine was increased, activation of ERK-p was increased while ERK level showed no significant difference as compared with that of control. Conclusions Protein tyrosine kinase, HER2 kinase, ERK kinase and PDGFR kinase pathway are important signal molecule and signal pathway. PI-3K pathway and p38MAPK have important function in anchorage-independent growth of the gastric cancer cells, but a lesser role in anchorage-independent survival.