China Oncology ›› 2015, Vol. 25 ›› Issue (12): 959-965.doi: 10.3969/j.issn.1007-3969.2015.12.007

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The effect of BTG1 overexpression on the proliferation and apoptosis of laryngeal cancer cells and its molecular mechanism in vitro

JIANG Runxue1, HU Wanning1, SUN Guogui2, LI Jun1, HAN Xiaochen1, CAI Haifeng1   

  1. 1.Department of Head and Neck Surgery, Tangshan People’s Hospital of Hebei United University, Tangshan 063000, Hebei Province, China; 2.Department of Chemoradiotherapy, Tangshan People’s Hospital of Hebei United University, Tangshan 063000, Hebei Province, China
  • Online:2015-12-30 Published:2016-02-03
  • Contact: HU Wanning E-mail: rmyy_hwn@163.com

Abstract: Background and purpose: B-cell translocation gene 1(BTG1) can inhibit cell proliferation, promote cell apoptosis and regulate cell cycle progression and differentiation in a variety of cell types. This study aimed to explore the influence on cell proliferation, apoptosis and cell cycle and its related mechanism of laryngeal cancer Hep - 2 cell lines through BTG1 overexpression by in vitro experiments. Methods: The BTG1 expression plasmids were constructed and transfected into Hep-2. They were divided into experimental group (transfected BTG1 of Hep-2 cells) and control group (transfected empty plasmid of Hep-2 cells). Western blot method was used to identify BTG1 protein expression levels of cells; proliferation activity of cells was detected by MTT assay; flow cytometry was used to analyze the cell cycle distribution and Annexin Ⅴ-FITC/PI cell apoptosis; Western blot was also used to assay cell cycle regulatory protein and apoptosis-related protein expression. Results: The pEGFP-N1-BTG1 plasmid was constructed successfully, and the expression of BTG1 protein was higher in experimental group than that in control group (0.921±0.091 vs 0.308±0.047, P<0.05). Compared with the two group of laryngeal cancer Hep-2 cells, the cell growth in experimental group was slowed down and the proliferation was reduced (P<0.05); Cyclin D1 protein expression level was decreased (0.436±0.023 vs 0.916±0.092, P<0.05), the proportion of G0/G1 phase cell cycle was increased [(85.1±5.2)% vs (63.8±3.1)%, P<0.05], the proportion of S phase cell was decreased [(8.3±1.1)% vs (23.1±1.5)%, P<0.05], phosphatidylserine ectropion in experimental group was increased, cell early apoptosis was significant [(10.3±1.1)% vs (2.8±0.3)%, P<0.05] and anti-apoptotic protein Bcl-2 expression level was reduced(0.167±0.009 vs 0.834±0.084, P<0.05). Conclusion: BTG1 high expression could inhibit the proliferation growth of laryngeal Hep-2 cells and promote its apoptosis, and the possible mechanisms are interrelated with BTG1 involved in cell cycle regulation and causing cell apoptosis.

Key words: Laryngeal cancer, BTG1, Proliferation, Apoptosis, Cell cycle