Abstract
The involvement of ERK signals in gastric carcinoma was investigated using Western blot, MTT, and flow cytometric analysis in cultured cells SGC7901. Results showed that treatment of sorafenib potently inhibited gastric SGC7901 cells proliferation, migration, invasion as well as promoted apoptosis. Treatment of sorafenib significantly decreased phosphorylation activation of ERK protein in a dose-dependent manner. Treatment of sorafenib still significantly increased caspase-3, bax, cyt-c protein expression and decreased bcl-2 protein in a dose-dependent manner. Our study confirms that ERK signals pathway is closely associated with development of gastric cancer. Deactivation of phosphorylation of ERK protein is one of the mechanisms of sorafenib inhibiting gastric cancer.
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