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Growth inhibition and underlying mechanisms following siRNA silencing of STAT3 in colorectal cancer SW480 cells
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Abstract:
Objective:To determine the effect of siRNA silencing of signal transducer and activators of transcription 3 ( STAT3) gene on proliferation/apoptosis, invasion, colony formation, and Mcl-1 and caspase3 expression of colorectal cancer SW480 cells in vitro. Methods: SW480 cells were infected by a GFP-STAT3-siRNA-carrying lentivirus vector or a GFP-carrying control vector. At 72 h after infection, mRNA and protein levels of STAT3, Mcl-1, and caspase3 were analyzed by Real-time PCR and Western blotting respectively, apoptosis by flow cytometry, the invasive activity by transwell assays in the infected SW480 cells. Results: The colony forming ability of SW480 cells was significantly suppressed after infection with the lentiviral vector carrying GFP-STAT3-siRNA as compared to the GFP-carrying control vector (P<005). Infection with the lentirival vector carrying GFP-STAT3-siRNA significantly decreased mRNA and protein levels of STAT3 and Mc1-1 (P<0.05), significantly increased mRNA and protein levels of caspase3 (P<0.05), significantly increased the percentage of apoptotic cells (11.9% vs 4.92%, P<0.05), and significantly reduced the invasive activity (178.49±15.42 vs 320.61±13.30, P<0.05) in SW480 cells as compared with the control vector infection. Conclusion: Silencing of the STAT3 gene in colorectal cancer cells promotes apoptosis and inhibits invasion and colony formation, possibly through modulating the expression of Mc1-1 and caspase3.
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Project Supported:
Project supported by the Basic Application and Cutting-edge Technology Research Project of Tianjin （No. 09JCYBJC11800)
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