Tianjin Medical Journal ›› 2019, Vol. 47 ›› Issue (7): 692-696.doi: 10.11958/20182237

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The effect and mechanism of OCCLUDIN on proliferation and apoptosis of SPC-A1 cells

YUAN Le-yong,WANG Mei-fang   

  1. 1 Department of Immunology, School of Basic Medical Sciences, Hubei University of Medical, Hubei 442000, China; 2 Department of Respiratory, the Affiliated Taihe Hospital of Hubei University of Medical
  • Received:2019-01-03 Revised:2019-04-17 Published:2019-07-15 Online:2019-08-01

Abstract: Objective To investigate the effect of OCCLUDIN on proliferation and apoptosis of SPC-A1 cells and its mechanism thereof. Methods Non-small cell lung cancer cell line SPC-A1 was cultured and interfered with OCCLUDIN expression by siRNA transfection. The cells were divided into blank control group (control group), idling group (siCtrl group)and siRNA transfection group (siOCLN group). The effects of OCCLUDIN on proliferation and apoptosis of SPC-A1 cells were detected by CCK-8 assay, flow cytometry and Western blot assay. Results The cell proliferation abilities of siOCLN cells were significantly lower at 24 h, 48 h, 72 h, 96 h and 120 h than those of control group and siCtrl group (P<0.05). The apoptosis rate was significantly higher in siOCLN group than that of control group and siCtrl group (P<0.05). The levels of apoptosis-related proteins such as Bax, caspase-3, caspase-9, AIF and Cyt C were significantly higher in siOCLN group than those in control group and siCtrl group (P<0.05). The level of anti-apoptotic protein Bcl-2 was significantly lower in siOCLN group than that of control group and siCtrl group (P<0.05). At the same time, the phosphorylation levels of AKT and PI3K protein were significantly lower in siOCLN group than those in control group and siCtrl group (P<0.05). Conclusion OCCLUDIN may promote the proliferation and inhibit apoptosis of SPC-A1 cells by regulating PI3K/AKT signaling pathway.

Key words: carcinoma, non-small-cell lung, tumor cells, cultured, occludin, phosphatidylinositol 3-kinases, cell proliferation, apoptosis