Zhao Zheng-Yuan, Han Chen-Guang, Liu Jun-Tao, Wang Chang-Lei, Wang Yi, Cheng Li-Ya
Department of General Thoracic Surgery, Affiliated Hospital of Logistics University of Chinese People's Armed Police Forces, Tianjin, China E-mail :
Asian Pac J Cancer Prev. 2013;14(11):6305-9. doi: 10.7314/apjcp.2013.14.11.6305.
TIAM2, a Rac guanine nucleotide exchange factor, is closely associated with cell adherence and migration. Here, we aimed to investigate the role of TIAM2 in non-small cell lung cancer (NSCLC) cells.
A small interference RNA (siRNA) was introduced to silence the expression of TIAM2. Invasion and motility assays were then performed to assess the invasion and motility potential of NSCLC cells. GST-pull down assays were used to detect activation of Rac1.
TIAM2 was highly expressed in NSCLC cells. Knockdown of TIAM2 inhibited the invasion and motility, and suppressed activation of Rac1. Further experiments demonstrated that knockdown of TIAM2 could up-regulate the expression of E-cadherin, and down- regulate the expression of MMP-3, Twist and Snail.
Our data suggest that TIAM2 can promote invasion and motility of NSCLC cells. Activation of Rac1 and regulation of some EMT/invasion-related genes may be involved in the underlying processes.
TIAM2是一种Rac鸟嘌呤核苷酸交换因子,与细胞黏附和迁移密切相关。在此,我们旨在研究TIAM2在非小细胞肺癌(NSCLC)细胞中的作用。
引入小干扰RNA(siRNA)以沉默TIAM2的表达。然后进行侵袭和运动性测定,以评估NSCLC细胞的侵袭和运动潜能。采用谷胱甘肽S-转移酶(GST)下拉实验检测Rac1的激活情况。
TIAM2在NSCLC细胞中高表达。TIAM2基因敲低抑制了侵袭和运动性,并抑制了Rac1的激活。进一步实验表明,TIAM2基因敲低可上调E-钙黏蛋白的表达,并下调基质金属蛋白酶-3(MMP-3)、Twist和Snail的表达。
我们的数据表明,TIAM2可促进NSCLC细胞的侵袭和运动性。Rac1的激活以及一些上皮-间质转化(EMT)/侵袭相关基因的调控可能参与了潜在的过程。