KIF3C Promotes the Malignant Progression of Lung Cancer Cells A549

Haiwang Liu, Ran Liu, Meiling Hao, Xing Zhao, Chunhui Li
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Abstract

Objective: To investigate the role of KIF3C gene in promoting the malignant phenotype of lung cancer cells and in regulating PI3K/AKT signaling pathway. Methods: CCK-8 and transwell assays were used to detect the changes in cell proliferation and cell migration ability after being transfected with siKIF3C, as well as the protein expression levels of PI3K, p-PI3K, AKT, and p-AKT following the downregulation of KIF3C by Western blot. Results: The CCK-8 assay showed that the proliferation/viability of lung cancer cells A549 significantly reduced after being transfected with siKIF3C gene (P < 0.05); the migration ability of lung cancer cells A549 was significantly reduced after transfected with siKIF3C gene (P < 0.05); the levels of p-PI3K and p-AKT proteins were downregulated after KIF3C protein knockdown (P < 0.05); however, the detection of PI3K and AKT protein levels was not statistically significant. Conclusion: KIF3C may promote the proliferation and migration ability of lung cancer cells A549 through PI3K/AKT signaling pathway.
KIF3C促进肺癌症细胞A549的恶性进展
目的:探讨KIF3C基因在促进肺癌细胞恶性表型及调控PI3K/AKT信号通路中的作用。方法:采用CCK-8法和transwell法检测转染siKIF3C后细胞增殖和细胞迁移能力的变化,以及Western blot检测KIF3C下调后PI3K、p-PI3K、AKT、p-AKT蛋白的表达水平。结果:CCK-8检测显示,转染siKIF3C基因后,肺癌细胞A549的增殖/活力显著降低(P < 0.05);转染siKIF3C基因后,肺癌细胞A549的迁移能力显著降低(P < 0.05);KIF3C蛋白敲低后,P - pi3k、P - akt蛋白水平下调(P < 0.05);而PI3K、AKT蛋白水平检测差异无统计学意义。结论:KIF3C可能通过PI3K/AKT信号通路促进肺癌细胞A549的增殖和迁移能力。
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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