Objective:To investigate the multiple molecular targeted agent, sorafenib, in human gastric cancer SGC-7901 cell proliferation, apoptosis and P-ERK expression, and explore its possible mechanism. Methods:MTT method was used to detect antiproliferative ratio of sorafenib on human gastric cancer SGC-7901 cell; immunocytochemical method for detection of gastric cancer cells P-ERK protein expression; and flow cytometry to analyze gastric cancer cell apoptosis. Results:Sorafenib obviously inhibited proliferation of gastric cancer cells and showed time-dose-dependent effects (P<0.05). When gastric cancer SGC-7901 cells were treated with sorafenib, immunocytochemistry showed that P-ERK expression was significantly decreased (P<0.05); flow cytometry showed that the SGC-7901 cell apoptosis rate increased (P<0.05). Conclusions:Sorafenib can significantly inhibit human gastric cancer SGC-7901 cell growth in vitro; the main mechanism is the inhibition of P-ERK expression, and thereby inhibit their proliferation and promote apoptosis.