The effect of BTG1 overexpression on the proliferation and apoptosis of laryngeal cancer cells and its molecular mechanismin vitro / 中国癌症杂志

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 inlfuence on cell proliferation, apoptosis and cell cycle and its related mechanism of laryngeal cancer Hep - 2 cell lines through BTG1 overexpression byin 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; lfow cytometry was used to analyze the cell cycle distribution and AnnexinⅤ-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±0.091vs 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±0.023vs 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±0.009vs 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.