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Sorafenib regulating ERK signals pathway in gastric cancer cell
Liu Wei Juan1, Lin Ming En2, Lin Hao3
1Department of Plastic Surgery, The First Affiliated Hospital of Shantou University Medical College, Shantou, PR China.
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.
Insights
Sorafenib effectively inhibits gastric cancer cell growth and spread by reducing ERK pathway activation. This mechanism involves promoting apoptosis and altering key protein expressions, offering a new therapeutic strategy for gastric carcinoma.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Gastric carcinoma is a significant global health concern.
- The Extracellular signal-Regulated Kinase (ERK) signaling pathway plays a crucial role in cancer development.
- Understanding the molecular mechanisms of targeted therapies is vital for improving gastric cancer treatment.
Purpose of the Study:
- To investigate the role of the ERK signaling pathway in gastric carcinoma.
- To elucidate the mechanism by which sorafenib inhibits gastric cancer cell progression.
Main Methods:
- Utilized cultured human gastric adenocarcinoma cells (SGC7901).
- Employed Western blot, MTT assay, and flow cytometric analysis.
- Assessed protein expression levels, including phosphorylated ERK, caspase-3, bax, cytochrome c, and bcl-2.
Main Results:
- Sorafenib significantly inhibited proliferation, migration, and invasion of SGC7901 cells.
- Sorafenib treatment dose-dependently decreased ERK phosphorylation.
- Sorafenib increased the expression of pro-apoptotic proteins (caspase-3, bax, cytochrome c) and decreased anti-apoptotic protein (bcl-2).
Conclusions:
- The ERK signaling pathway is closely associated with the development of gastric cancer.
- Inhibition of gastric cancer progression by sorafenib is partly mediated by the deactivation of ERK phosphorylation.
- These findings highlight the therapeutic potential of targeting the ERK pathway in gastric cancer treatment.
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