The Effects and Mechanism of IscU2 on Cell Proliferation, Migration and Invasion Ability in Non-small Cell Lung Cancer Cells
HAN Qinxia1, SUN Qianqian1,2, LIN Zifan1, ZHOU Huaibin1, LÜ Jianxin1*
In this study, IscU2 was knocked down by shRNA interference technology in NSCLC NCI-H520 cell lines, and then we investigated the effects of IscU2 interference on cell proliferation, migration and invasion ability in NSCLC (non-small cell lung cancer) cells. The proliferation ability was detected by CCK-8 and colony formation assay. The changes of cell cycle, apoptosis, ROS and mitochondrial membrane potential were detected by flow cytometry. Transwell assay was used to detect cell migration and invision. Western blot was used to detect protein expression. The experiment results showed that when we inhibited the expression of IscU2 in NSCLC cells, the cell proliferation and colony formation ability were significantly lower than that of control group. Cell cycle was blocked at G1/G0 phase, and the expression of p-AKT and Cyclin D1 was downregulated. Meanwhile, the rate of late apoptosis was obviously increased, Cleaved-caspase3 and Cleaved-PARP, the key proteins of apoptosis were significantly upregulated. In addition, the cell migration and invision capacity were decreased, the epithelial marker E-Cadherin protein was increased and the mesenchymal markers, N-Cadherin and Snail proteins were reduced. Furthermore, it resulted in the accumulation of ROS and decreased the mitochondrial membrane potential. These results indicated that knockdown of IscU2 obviously inhibit the proliferation, migration and invision ability in NSCLC cells, which provide new potential targets and perspectives for treatment of non-small cell lung cancer.
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