Department of Thoracic Surgery, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Department of Anesthesiology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Chin J Physiol. 2023 Nov-Dec;66(6):456-465. doi: 10.4103/cjop.CJOP-D-22-00124.
Recently, evidence has shown that microRNA-100-3p (miR-100-3p) has been revealed as a tumor suppressor in diverse human diseases, while its capability in lung cancer warrants further validation. In this work, we aimed to discuss the impact of sevoflurane on biological functions of lung cancer cells by modulating the miR-100-3p/sterol O-acyltransferase 1 (SOAT1) axis. Lung cancer cell lines (A549 and H460) were treated with various concentrations of sevoflurane. Cell viability, proliferation, migration, and invasion were evaluated using MTT, colony formation, wound healing, and transwell assays. Moreover, miR-100-3p and SOAT1 expressions were evaluated by reverse transcription-quantitative polymerase chain reaction in lung cancer cells. The target interaction between miR-100-3p and SOAT1 was predicted by bioinformatics analysis and verified by the dual-luciferase reporter gene assay. The findings of our work demonstrated that sevoflurane impeded the abilities on viability, proliferation, migration, and invasion of A549 and H460 cells. The expression of miR-100-3p was reduced, and SOAT1 expression was elevated in lung cancer cells. miR-100-3p targeted SOAT1. Besides, sevoflurane could lead to expressed improvement of miR-100-3p or limitation of SOAT1. Downregulation of miR-100-3p or upregulation of SOAT1 restored the suppression of sevoflurane on abilities of viability, proliferation, migration, and invasion in A549 and H460 cells. In the rescue experiment, downregulation of SOAT1 reversed the impacts of downregulation of miR-100-3p on sevoflurane on lung cancer cells. Collectively, our study provides evidence that sevoflurane restrained the proliferation and invasion in lung cancer cells by modulating the miR-100-3p/SOAT1 axis. This article provides a new idea for further study of the pathogenesis of lung cancer.
最近的证据表明，微小 RNA-100-3p（miR-100-3p）在多种人类疾病中被揭示为肿瘤抑制因子，而其在肺癌中的作用仍需进一步验证。在这项工作中，我们旨在通过调节 miR-100-3p/固醇 O-酰基转移酶 1（SOAT1）轴来讨论七氟醚对肺癌细胞生物学功能的影响。用不同浓度的七氟醚处理肺癌细胞系（A549 和 H460）。通过 MTT、集落形成、划痕愈合和 Transwell 测定评估细胞活力、增殖、迁移和侵袭。此外，通过逆转录定量聚合酶链反应评估肺癌细胞中 miR-100-3p 和 SOAT1 的表达。通过生物信息学分析预测 miR-100-3p 和 SOAT1 之间的靶相互作用，并通过双荧光素酶报告基因测定进行验证。我们的研究结果表明，七氟醚抑制了 A549 和 H460 细胞的活力、增殖、迁移和侵袭能力。肺癌细胞中 miR-100-3p 的表达减少，SOAT1 的表达增加。miR-100-3p 靶向 SOAT1。此外，七氟醚可导致 miR-100-3p 的表达改善或 SOAT1 的表达受限。下调 miR-100-3p 或上调 SOAT1 可恢复七氟醚对 A549 和 H460 细胞活力、增殖、迁移和侵袭能力的抑制作用。在挽救实验中，下调 SOAT1 逆转了下调 miR-100-3p 对七氟醚对肺癌细胞的影响。综上所述，我们的研究表明，七氟醚通过调节 miR-100-3p/SOAT1 轴抑制肺癌细胞的增殖和侵袭。这为进一步研究肺癌的发病机制提供了新的思路。
