Xing R, He H, He Y, Feng Y, Zhang C, Wu H, Sun M, Yu X, Liu Y, Song X, Wang X, Chen Y, Hou Y
Department of Cell Biology, College of Life Sciences, Shaanxi Normal University, Shaanxi, China.
Cell Mol Biol (Noisy-le-grand). 2013 Feb 26;59 Suppl:OL1848-54.
ANXA2 was reported as a multiple tumors relevant gene expressed excessively in many tumor tissue types, especially in the cancers from digestion system, and its aberrant expression enhances the malignant properties of cancer cells. We suppose that the microstructure heterogeneity is important to maintain the malignancy of cancer cells, and excessive ANXA2 expression enhance the malignancy by remodeling the microstructures of cancer cells. To validate the proposal, the ANXA2-/-caco2 cell line was generated and the changes of the microstructures in the ANXA2 deleted and wild type caco2 cells were observed under fluorescence microscope, laser scanning confocal microscope and electron microscope. We found that ANXA2 deletion induced the pseudopodia shorted and spared, non-stained areas increased, mitochondria decreased, and the expression and polymerization of F-actin and β-tubulin changed. By the findings above, it is firstly reported in this paper that the ANXA2 excessive expression induces the significant changes of the microstructures in cancer cells. Combining our previous data together, our results indicate that ANXA2 excessive expression enhances the malignancy of cancers partially by remodeling the cell microstructures.
膜联蛋白A2(ANXA2)被报道为一种与多种肿瘤相关的基因,在许多肿瘤组织类型中过度表达,尤其是在消化系统癌症中,其异常表达增强了癌细胞的恶性特性。我们推测微观结构异质性对于维持癌细胞的恶性程度很重要,而ANXA2的过度表达通过重塑癌细胞的微观结构来增强恶性程度。为了验证这一推测,我们构建了ANXA2基因敲除的caco2细胞系,并在荧光显微镜、激光扫描共聚焦显微镜和电子显微镜下观察了ANXA2缺失的caco2细胞和野生型caco2细胞微观结构的变化。我们发现ANXA2缺失导致伪足变短且稀疏、不着色区域增加、线粒体减少,并且F-肌动蛋白和β-微管蛋白的表达及聚合发生改变。基于上述发现,本文首次报道ANXA2的过度表达会诱导癌细胞微观结构发生显著变化。结合我们之前的数据,我们的结果表明ANXA2的过度表达部分通过重塑细胞微观结构来增强癌症的恶性程度。