2011•Unpublished venueRequires access

The effect of sorafenib on growth,apoptosis and P-ERK expression in human gastric cancer SGC-7901 cells

Liangqing Li

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Abstract

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(P0.05).When gastric cancer SGC-7901 cells were treated with sorafenib,immunocytochemistry showed that P-ERK expression was significantly decreased(P0.05);flow cytometry showed that the SGC-7901 cell apoptosis rate increased(P0.05).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.

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What this paper is about

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(P0.05).When gastric cancer SGC-7901 cells were treated with sorafenib,immunocytochemistry showed that P-ERK expression was significantly decreased(P0.05);flow cytometry showed that the SGC-7901 cell apoptosis rate increased(P0.05).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.

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Available abstract

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(P0.05).When gastric cancer SGC-7901 cells were treated with sorafenib,immunocytochemistry showed that P-ERK expression was significantly decreased(P0.05);flow cytometry showed that the SGC-7901 cell apoptosis rate increased(P0.05).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.

Key concepts: Sorafenib, Apoptosis, MAPK/ERK pathway, Medicine, Flow cytometry, Cell growth, Cancer, Cancer cell

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The effect of sorafenib on growth,apoptosis and P-ERK expression in human gastric cancer SGC-7901 cells — Research Paper | ScholarLens