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作 者:张可[1] 朱卿文 益欢欢 僧东杰 ZHANG Ke;ZHU Qing-wen;YI Huan-huan;SENG Dong-jie(Department of Otolaryngology of Head and Neck Surgery,Zhengzhou Children's Hospital/He'nan Children's Hospital/Affiliated Children's Hospital of Zhengzhou University,Zhengzhou 450018,China)
机构地区:[1]郑州大学附属儿童医院/河南省儿童医院/郑州儿童医院耳鼻咽喉头颈外科,郑州450018
出 处:《循证医学》2022年第3期163-168,共6页The Journal of Evidence-Based Medicine
基 金:2019年度河南省医学攻关计划联合共建项目(LHGJ20190954)。
摘 要:目的研究微管相关蛋白(targeting protein for Xenopus kinesin-like protein 2,TPX2)在鼻咽癌增殖和转移中的作用及可能的分子机制。方法构建TPX2si RNA质粒,同时设置空载对照,转染人鼻咽癌细胞CNE2Z,采用CCK-8检测细胞增殖情况,Transwell试验检测细胞的迁移和侵袭能力,Western blot法检测细胞周期相关蛋白表达情况和EMT标志物的表达变化。结果TPX2si RNA转染能够显著抑制CNE2Z细胞中TPX2的表达,CCK-8分析发现TPX2的干扰会显著抑制CNE2Z细胞增殖,Western blot分析发现细胞周期蛋白中cyclin D1、cyclin E下调,p27上调;Transwell试验分析发现TPX2的干扰会显著抑制细胞的侵袭;Western blot分析发现TPX2干扰后,EMT通路相关指标检测分析发现上皮细胞分子标志物E-cadherin上调,间质细胞分子标志物Vimentin-N下调。结论TPX2抑制了CNE2Z细胞的增殖、迁移、侵袭,随着TPX2在鼻咽癌中调控机制的深入研究,TPX2有望成为鼻咽癌诊断和治疗的新靶点。Objective To investigate the role of microtubule-associated protein(targeting protein for Xenopus kinesinlike protein 2,TPX2)in the proliferation and metastasis of nasopharyngeal carcinoma and its possible molecular mechanism.Methods The TPX2si RNA plasmid was constructed,and a no-load control was set at the same time.The cells were transfected into human nasopharyngeal carcinoma cells CNE2Z.The cell proliferation was detected by CCK-8 and the cell proliferation was detected by the Transwell test.The expression of cell cycle related proteins and EMT markers were detected by Western blot.Results TPX2si RNA transfection can significantly inhibit the expression of TPX2 in CNE2Z cells.CCK-8 analysis found that the interference of TPX2 significantly inhibited the proliferation of CNE2Z cells.Western blot analysis showed that cyclin D1 and cyclin E were down-regulated and p27 was up-regulated in cyclin.Transwell test analysis found that interference of TPX2 can significantly inhibit cell invasion.Western blot analysis showed that after TPX2 interference,EMT pathway related indicators analysis showed that the epithelial cell molecular marker E-cadherin was up-regulated,and the stromal cell molecular marker Vimentin-N was down-regulated.Conclusions TPX2 has an important effect on the proliferation,migration,and invasion of CNE2Z cells.With the further study of the regulation mechanism of TPX2 in nasopharyngeal carcinoma,TPX2 was expected to become a new target for diagnosis and treatment of nasopharyngeal carcinoma.
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