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索托拉西布与二甲双胍的联合应用通过抑制 MAPK 和 P70S6K 增强 KRAS 突变型非小细胞肺癌细胞系的细胞毒性和细胞凋亡。

A Novel Combination of Sotorasib and Metformin Enhances Cytotoxicity and Apoptosis in KRAS-Mutated Non-Small Cell Lung Cancer Cell Lines through MAPK and P70S6K Inhibition.

机构信息

Thoracic Oncology Functional Unit (UFOT), Laboratorio de Medicina Personalizada, Instituto Nacional de Cancerología, S.S.A., San Fernando 22 Sección XVI, Tlalpan, Mexico City 14080, Mexico.

出版信息

Int J Mol Sci. 2023 Feb 22;24(5):4331. doi: 10.3390/ijms24054331.

Abstract

Novel inhibitors of KRAS with G12C mutation (sotorasib) have demonstrated short-lasting responses due to resistance mediated by the AKT-mTOR-P70S6K pathway. In this context, metformin is a promising candidate to break this resistance by inhibiting mTOR and P70S6K. Therefore, this project aimed to explore the effects of the combination of sotorasib and metformin on cytotoxicity, apoptosis, and the activity of the MAPK and mTOR pathways. We created dose-effect curves to determine the IC50 concentration of sotorasib, and IC10 of metformin in three lung cancer cell lines; A549 (KRAS G12S), H522 (wild-type KRAS), and H23 (KRAS G12C). Cellular cytotoxicity was evaluated by an MTT assay, apoptosis induction through flow cytometry, and MAPK and mTOR pathways were assessed by Western blot. Our results showed a sensitizing effect of metformin on sotorasib effect in cells with KRAS mutations and a slight sensitizing effect in cells without K-RAS mutations. Furthermore, we observed a synergic effect on cytotoxicity and apoptosis induction, as well as a notable inhibition of the MAPK and AKT-mTOR pathways after treatment with the combination, predominantly in KRAS-mutated cells (H23 and A549). The combination of metformin with sotorasib synergistically enhanced cytotoxicity and apoptosis induction in lung cancer cells, regardless of KRAS mutational status.

摘要

新型 KRAS G12C 突变抑制剂(索托拉西布)由于 AKT-mTOR-P70S6K 通路介导的耐药性而导致短暂的反应。在这种情况下,二甲双胍通过抑制 mTOR 和 P70S6K 成为打破这种耐药性的有前途的候选药物。因此,本项目旨在探索索托拉西布和二甲双胍联合使用对细胞毒性、细胞凋亡以及 MAPK 和 mTOR 通路活性的影响。我们创建了剂量-效应曲线来确定三种肺癌细胞系(A549[KRAS G12S]、H522[野生型 KRAS]和 H23[KRAS G12C])中索托拉西布的 IC50 浓度和二甲双胍的 IC10。通过 MTT 测定法评估细胞毒性,通过流式细胞术诱导细胞凋亡,并通过 Western blot 评估 MAPK 和 mTOR 通路。我们的结果表明,二甲双胍对具有 KRAS 突变的细胞中索托拉西布的作用具有增敏作用,对没有 K-RAS 突变的细胞具有轻微的增敏作用。此外,我们观察到联合用药后在细胞毒性和细胞凋亡诱导方面具有协同作用,以及 MAPK 和 AKT-mTOR 通路的显著抑制,尤其是在 KRAS 突变细胞(H23 和 A549)中。二甲双胍与索托拉西布联合使用可协同增强肺癌细胞的细胞毒性和细胞凋亡诱导作用,而与 KRAS 突变状态无关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53b8/10001819/9c6162ded3ca/ijms-24-04331-g001.jpg

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