細胞および分子生物学

抽象的な

KIAA0101 Silencing Overcomes Cisplatin Resistance in Non-Small Cell Lung Cancer by Inhibiting PI3K/AKT/mTOR Pathway

Mingming Zhang

We constructed KIAA0101 overexpression plasmids and KIAA0101 interference plasmids. MTT assay was used to detect the effect of KIAA0101 knockdown and overexpression on NSCLC cell resistance to cisplatin. Finally, we explore the regulating mechanism of KIAA0101 regulating cisplatin resistance in NSCLC by WB and the rescue experiment. Our research showed that cisplatin had much stronger inhibitory effects, cisplatin-resistance level decreased, and the expression of PI3K, p-Akt, and p-mTOR significantly decreased in NSCLC cells when KIAA0101 expression was knocked down. On the contrary, overexpression of KIAA0101 significantly weakens the inhibitory effect of cisplatin on NSCLC cells, and cisplatin-resistance level, while the expression of PI3K, p-Akt, and p-mTOR significantly increased. When adding PI3K signaling pathway inhibitor wortmannin on the overexpressing of KIAA0101, the role of KIAA0101 in enhancing lung cancer resistance was reversed, and the expression of PI3K, p-AKT, and p-mTOR protein decreased. Our study revealed for the first time that KIAA0101 as a carcinogen promoting cisplatin resistance in NSCLC, and may be regarded as a new target for clinical treatment of non-small cell lung cancer.