TCF21对喉癌Hep-2细胞生物学行为的影响

摘要

目的:探讨转录因子21(transcription factor 21,TCF21)对喉癌细胞株Hep-2生物学特性的影响及其相关的作用机制.方法:利用慢病毒转染技术外源性过表达喉癌Hep-2细胞中的TCF21,然后分别采用细胞增殖检测(Cell Counting Kit-8,CCK-8)法和流式细胞术检测细胞增殖及凋亡能力的变化;Western印迹检测周期及凋亡相关蛋白的表达.结果:在Hep-2细胞中过表达TCF21后,细胞的增殖能力显著降低,周期进程缓慢,而细胞凋亡显著增加;Transwell细胞迁移实验显示过表达TCF21可抑制Hep-2细胞迁移.Western印迹实验结果显示过表达TCF21后,cyclinD1,CDK4,CDK6,p-Rb及bcl-2的蛋白表达水平显著下降;P21和Bax及cleaved-caspase-3的蛋白表达水平显著升高.结论:人喉癌细胞株Hep-2中,过表达TCF21可通过调控周期及凋亡相关因子的表达,发挥增殖抑制及凋亡促进作用,提示TCF21可作为诊断和靶向治疗喉癌的潜在作用位点.%Objective: To investigate the effect and mechanism of transcription factor 21 (TCF21) on the cellular biological characteristics in laryngeal carcinoma cell line Hep-2. Methods: Lentiviral transfection was used to up-regulated TCF21 expression in Hep-2 cells, and then cell proliferation and apoptosis were detected with Cell Counting Kit-8 (CCK-8) assay and flow cytometry assay, respectively. The expression of cell cycle- and apoptosis-related molecules at protein level was measured by Western blot. Results: Over-expression of TCF21 suppressed cell proliferation and cell cycle, while promoted cell apoptosis in Hep-2 cell (P<0.05). Western blot showed that the expression of cyclinD1, CDK4, CDK6, p-Rb and Bcl-2 at protein level decreased significantly after up-regulation of TCF21, with an increased expression of P21, Bax and cleaved-caspase-3 (P<0.05). Conclusion: In Hep-2 cells, over-expression of TCF21 could suppress cell proliferation and cell cycle, while promote cell apoptosis via regulating the expression of cell cycle- and apoptosis-related molecules, suggesting that TCF21 may be a potential new target for diagnosis and targeted therapy of laryngeal carcinoma.