OBJECTIVE To investigate the effects of L-Se-methylselenocysteine(L-SeMC) on apoptosis and apoptosis-related proteins in esophageal cancer EC9706 cells, and to explore the mechanism of its apoptosis induction.

METHODS Different concentrations of L-SeMC(12.5, 25, 50, 100, 200 μmol·L⁻¹) RPMI-1640 were treated on EC9706 cells for 24 h and 48 h, and the inhibitory effect of L-SeMC on cell proliferation was detected by MTT assay. The migration of esophageal cancer EC9706 cells after intervention with different concentrations of L-SeMC was detected by scratch test. The apoptosis of esophageal cancer EC9706 cells after intervention with L-SeMC(blank, 25, 50, 100 μmol·L⁻¹) was detected by flow cytometry. Western blotting assay was used to detect Bcl-2, Bax, Caspase 3, PI3K, AKT, p-PI3K, p-AKT protein expression.

RESULTS L-SeMC significantly inhibited the proliferation of EC9706 cells in a time-concentration dependent manner(P<0.01), and the inhibition of 200 μmol·L⁻¹ was the most significant. After 48 h, the expressions of apoptosis-related proteins Bax and Caspase 3 in L-SeMC group were significantly up-regulated compared with the blank group(P<0.01), while the expression of Bcl-2 was significantly down-regulated compared with the blank group(P<0.01 or P<0.001), which was in a concentration dependent manner. Compared with blank group, L-SeMC group had no significant regulatory effect on PI3K and AKT protein, but significantly down-regulated pathway protein p-PI3K level(P<0.01 or P<0.001), L-SeMC(50 and 100 μmol·L⁻¹) significantly down-regulated pathway protein p-AKT level(P<0.001).

CONCLUSION L-SeMC can inhibit the proliferation and induce the apoptosis of human esophageal carcinoma cells EC9706 in a time-concentration dependent manner, its mechanism may be related to the inhibition of PI3K/AKT pathway.