TCTP silencing in ovarian cancer cells results in actin cytoskeleton remodeling and motility increase

Yianzhu Liu, Li Zhang, N. Tejpal, J. Kubiak, R. Ghobrial, X. Li, M. Kloc
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引用次数: 1

Abstract

Translationally Controlled Tumor-associated Protein (TCTP) plays a role in a plethora of normal and cancer cell functions including cell cycle progression, cell growth and metastasis. Our previous studies showed that TCTP interacts with cellular cytoskeleton and is localized, in cell-type specific manner, on actin filaments in various types of ovarian cancer cells. Here we used small interfering RNA (siRNA) for silencing TCTP expression in human ovarian surface epithelial noncancerous cell line HIO180, ovarian carcinoma cell lines SKOV3 and OVCAR3 and analyzed effect of TCTP silencing on actin cytoskeleton and cell motility. We show that a down regulation of TCTP caused dramatic restructuring and redistribution of actin filaments in HIO180, SKOV3 and OVCAR3 cells and resulted in cell motility increase. This previously unidentified dependence of actin cytoskeleton remodeling and cell motility on TCTP level might be responsible for high metastatic potential and aggressiveness of ovarian cancer cells and will help to pinpoint novel targets for anticancer therapies .
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卵巢癌细胞中TCTP沉默导致肌动蛋白细胞骨架重塑和运动性增加
翻译控制肿瘤相关蛋白(TCTP)在细胞周期进程、细胞生长和转移等多种正常细胞和癌细胞功能中发挥重要作用。我们之前的研究表明,TCTP与细胞骨架相互作用,并以细胞类型特异性的方式定位于各种类型卵巢癌细胞的肌动蛋白丝上。本实验采用小干扰RNA (siRNA)沉默人卵巢表面上皮非癌细胞系HIO180、卵巢癌细胞系SKOV3和OVCAR3中TCTP的表达,分析TCTP沉默对肌动蛋白细胞骨架和细胞运动的影响。我们发现,TCTP的下调导致HIO180、SKOV3和OVCAR3细胞中肌动蛋白丝的重组和重新分配,并导致细胞运动增加。这种先前未被发现的肌动蛋白细胞骨架重塑和细胞运动对TCTP水平的依赖性可能是卵巢癌细胞高转移性和侵袭性的原因,并将有助于确定抗癌治疗的新靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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