Abstract
This investigation aimed to determine effects of celecoxib on the cell cycle kinetics of the gastric cancer cell line MGC803 and the mechanisms involved by assessing expression of cytochrome C and caspase-9 at the protein level. Cell proliferation of MGC803 was determined by MTT assay after treatment with celecoxib. Apoptosis was assessed using fluorescence staining and cell cycle kinetics by flow cytometry. Western blotting was used to detect the expression of caspase-9 protein and of cytochrome C protein in cell cytosol and mitochondria. Celecoxib was able to restrain proliferation and induce apoptosis in a dose- and time- dependent manner, inducing G0/G1 cell cycle arrest, release of cytochrome C into the cytosol, and cleavage of pro-caspase-9 into its active form. Celecoxib can induce apoptosis in MGC803 cells through a mechanism involving cell cycle arrest, mitochondrial cytochrome C release and caspase activation.
Highlights
Gastric cancer is the second most common cause of cancer-associated death in the world
This investigation aimed to determine effects of celecoxib on the cell cycle kinetics of the gastric cancer cell line MGC803 and the mechanisms involved by assessing expression of cytochrome C and caspase-9 at the protein level
These findings suggest that COX-2 may play a key role in carcinogenesis and makes it a potential target in cancer therapy (Ghosh et al, 2010; Khan et al, 2011)
Summary
Gastric cancer is the second most common cause of cancer-associated death in the world. COX-2 is linked to tumor-promoting effects, including tumor growth and metastasis, by stimulating invasiveness and angiogenesis (Chen et al, 2009; Liu et al, 2011), inhibiting apoptosis and immune surveillance (Ohno et al, 2005), and enhancing drug resistance (Mehar et al, 2008). These findings suggest that COX-2 may play a key role in carcinogenesis and makes it a potential target in cancer therapy (Ghosh et al, 2010; Khan et al, 2011). In this study we investigated the effect of Celecoxib on the cell cycle kinetics of gastric cancer cell line MGC803 and the probable mechanism by examining the expressions of cytochrome C and Caspase-9 at protein level
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