Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts
Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts
复制标题
STIM1表达的敲低可抑制体外和裸鼠异种移植物中非小细胞肺癌细胞的增殖
DOI：
10.1080/21655979.2019.1669518
复制
发表时间：
2019-01-01
期刊：
影响因子：
4.9
通讯作者：
Song, Xin
中科院分区：
文献类型：
--
作者：
Ge, Chunlei;Zeng, Baozhen;Song, Xin
基质相互作用分子1（Stromal interaction molecule 1，STIM 1）是一种定位于内质网膜的钙敏感蛋白。STIM 1的表达与细胞增殖密切相关。本研究的目的是研究STIM 1在调节癌症进展及其临床相关性中的作用。数据表明，STIM 1在非小细胞肺癌（NSCLC）组织中的表达显著高于良性病变，并与晚期NSCLC T分期相关。在NSCLC细胞系A549和SK-MES-1中STIM 1表达的敲低显著抑制细胞增殖，并诱导A549和SK-MES-1细胞停滞在细胞周期的G2/M和S期。Western blotting结果显示，STIM 1基因表达下调后，细胞周期蛋白依赖性激酶（CDK）1和CDK 2的表达均降低。此外，NSCLC细胞中STIM 1的敲低显著降低了裸鼠中异种移植肿瘤生长的水平。这些数据表明，STIM 1蛋白的异常表达可能有助于NSCLC进展。未来的研究应将STIM 1作为NSCLC治疗的新策略。
Stromal interaction molecule 1 (STIM1) is a calcium-sensing protein localized in the membrane of the endoplasmic reticulum. The expression of STIM1 has been shown to be closely associated with cell proliferation. The aim of the present study was to investigate the role of STIM1 in the regulation of cancer progression and its clinical relevance. The data demonstrated that the expression of the STIM1 was significantly higher in non-small-cell lung cancer (NSCLC) tissues than in benign lesions and was associated with advanced NSCLC T stage. Knockdown of STIM1 expression in NSCLC cell lines A549 and SK-MES-1 significantly inhibited cell proliferation and induces A549 and SK-MES-1 cell arrest at the G2/M and S phases of the cell cycle. Western blotting showed that the expression of cyclin-dependent kinase (CDK) 1 and CDK2 were reduced while knockdown of STIM1 expression. Furthermore, knockdown of STIM1 in NSCLC cells significantly reduced the levels of xenograft tumor growth in nude mice. These data indicate that aberrant expression of the STIM1 protein may contribute to NSCLC progression. Future studies should focus on targeting STIM1 as a novel strategy for NSCLC therapy.