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《Immunological Journal》 2019-04
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LAMA4 regulates immune escape factors and promotes apoptosis of hepatocellular carcinoma cells through TGF-β1/SMAD signaling pathway

MA Liping;LIU Xiaolin;ZHANG Zhexiong;LI Xueyu;ZHOU Hong;Department of Laboratory Medicine, School of Medicine, Jiangsu University;Laboratory Department, Lianyungang Second People's Hospital;  
This study was performed to investigate the mechanism of LAMA4 affecting immune escape and apoptosis of hepatoma cells by regulating TGF-β1/SMAD signaling pathway. RT-qPCR and Western blot were used to detect the expression of LAMA4 in Huh7 cells, HepG2 cells and Human hepatocytes L02; MTT and flow cytometry assays were performed to analyze the effects of LAMA4 and TGF-β1/SMAD signaling pathway on the cell proliferation and apoptosis in Huh7 cells. RT-qPCR and Western blot were performed to analyze the effect of LAMA4 on TGF-β1/SMAD signaling pathway and cellular immune factors IFN-γ, TNF-α and TGF-β1. Data showed that the expression of LAMA4 was significantly upregulated in Huh7 and HepG2 cells. LAMA4 knockdown significantly increased the expression of TGF-β1 and SMAD4, while decreased the expression of SMAD6, IFN-γand TNF-α, which could be reversed by overexpression of LAMA4. MMT and flow cytometry showed that LAMA4 knockdown inhibited proliferation and induced apoptosis in Huh7 cells, while LAMA4 overexpression demonstrated the opposite effect. Ly364947 increased the expression of IFN-γ and TNF-α, decreased the expression of TGF-β1, promoted proliferation and blocked apoptosis by interfering the TGF-β1/SMAD signaling pathway in Huh7 cells. Ly364947 could partially reverse the effect of LAMA4 silence on cell immune escape factors and cell apoptosis in Huh7 cells. In conclusion, LAMA4 is involved in the immune escape and apoptosis of hepatoma carcinoma cell by regulating the TGF-β1/SMAD signaling pathway.
【CateGory Index】: R735.7
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