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Karyopherin alpha 2 induces apoptosis in tongue squamous cell carcinoma CAL-27 cells through the p53 pathway

机译:核转运蛋白α2通过p53途径诱导舌鳞癌CAL-27细胞凋亡

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摘要

Tumor onset and progression are associated with dysfunction of the nuclear transport machinery at the level of import and export receptors. However, the role of Karyopherin alpha 2 (KPNA2) in human tongue squamous cell carcinoma (TSCC) remains unknown. We assessed the proliferation, apoptosis and migration of TSCC CAL-27 cells using wound healing, Transwell and MTT assays, western blotting, electron microscopy and acridine orange/ethidium bromide staining following knockdown of KPNA2. The results revealed the antiproliferative, proapoptotic and anti-migratory effects of KPNA2 silencing on the TSCC CAL-27 cells. Moreover, the knockdown of KPNA2 proved to be accompanied by the upregulation of active caspase-3, cytochrome c, Bax, Bad and decreased expression of Bcl-2, p-Bad and XIAP. KPNA2 activated the caspase-dependent pathway in the CAL-27 cells with upregulation of p53, p21(Cip1/Waf1) and p16(INK4a). Thus, the present study demonstrated that p53/p21(Cip1/Waf1)/p16(INK4a) may be an important pathway involved in the function of KPNA2 in TSCC CAL-27 cells.
机译:在进出口受体的水平上,肿瘤的发生和发展与核运输机械的功能障碍有关。但是,Karyopherin alpha 2(KPNA2)在人舌鳞状细胞癌(TSCC)中的作用仍然未知。我们使用KPNA2敲除后,使用伤口愈合,Transwell和MTT分析,蛋白质印迹,电子显微镜和a啶橙/溴化乙锭染色法评估了TSCC CAL-27细胞的增殖,凋亡和迁移。结果揭示了KPNA2沉默对TSCC CAL-27细胞的抗增殖,促凋亡和抗迁移作用。此外,KPNA2的敲除被证明与活性caspase-3,细胞色素c,Bax,Bad的上调和Bcl-2,p-Bad和XIAP的表达降低有关。 KPNA2激活CAL-27细胞中的caspase依赖性途径,并上调p53,p21(Cip1 / Waf1)和p16(INK4a)。因此,本研究证明p53 / p21(Cip1 / Waf1)/ p16(INK4a)可能是参与TSCC CAL-27细胞中KPNA2功能的重要途径。

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