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异氟烷通过靶向miR-216抑制结肠癌细胞的增殖、迁移和侵袭并促进其凋亡。

Isoflurane Suppresses Proliferation, Migration, and Invasion and Facilitates Apoptosis in Colorectal Cancer Cells Through Targeting miR-216.

作者信息

Cai Zhe, Suo Liangyuan, Huang Zeqing

机构信息

Department of Anesthesiology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, China.

出版信息

Front Med (Lausanne). 2021 Aug 11;8:658926. doi: 10.3389/fmed.2021.658926. eCollection 2021.

Abstract

Surgery is the first line treatment of colorectal cancer (CRC). Anesthetic isoflurane may improve outcomes of cancer surgery. Herein, we investigated the effects of isoflurane on malignant behaviors of CRC cells and its underlying therapeutic target. SW620 and HCT116 CRC cells were exposed to a series of concentrations of isoflurane. CCK-8 assay was utilized for determination of the optimal concentration of isoflurane. Under treatment with isoflurane, proliferation, migration, and invasion were separately assessed via clone formation and transwell assays. Apoptotic levels were observed via flow cytometry and expression of Bax, Bcl-2, and Caspase3 proteins was quantified through western blot. MiR-216 expression was detected in isoflurane-induced SW620 and HCT116 cells by RT-qPCR. Following transfection with miR-216 mimic, malignant biological behaviors were examined in isoflurane-treated SW620 and HCT116 cells. 40 μM isoflurane distinctly restrained proliferative, migrated, and invasive capacities and elevated apoptotic levels in SW620 and HCT116 cells. Up-regulation of miR-216 was found in CRC cells. Its expression was suppressed by isoflurane. MiR-216 mimic ameliorated the reduction in proliferation, migration, and invasion and the increase in apoptosis for 40 μM isoflurane-induced SW620 and HCT116 cells. Isoflurane, a promising drug of CRC, may suppress malignant biological behaviors of tumor cells. Furthermore, miR-216 is an underlying target of isoflurane. Thus, isoflurane could be adopted for CRC treatment.

摘要

手术是结直肠癌(CRC)的一线治疗方法。麻醉剂异氟烷可能会改善癌症手术的效果。在此,我们研究了异氟烷对CRC细胞恶性行为的影响及其潜在的治疗靶点。将SW620和HCT116 CRC细胞暴露于一系列浓度的异氟烷中。采用CCK-8法测定异氟烷的最佳浓度。在用异氟烷处理后,通过克隆形成和Transwell实验分别评估细胞的增殖、迁移和侵袭能力。通过流式细胞术观察细胞凋亡水平,并通过蛋白质印迹法定量检测Bax、Bcl-2和Caspase3蛋白的表达。通过RT-qPCR检测异氟烷诱导的SW620和HCT116细胞中miR-216的表达。在用miR-216模拟物转染后,检测异氟烷处理的SW620和HCT116细胞中的恶性生物学行为。40μM异氟烷明显抑制了SW620和HCT116细胞的增殖、迁移和侵袭能力,并提高了细胞凋亡水平。在CRC细胞中发现miR-216上调。其表达受到异氟烷的抑制。miR-216模拟物改善了40μM异氟烷诱导的SW620和HCT116细胞增殖、迁移和侵袭的减少以及细胞凋亡的增加。异氟烷是一种有前景的CRC治疗药物,可能抑制肿瘤细胞的恶性生物学行为。此外,miR-216是异氟烷的潜在靶点。因此,异氟烷可用于CRC治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148f/8385302/159a0d9afe5d/fmed-08-658926-g0001.jpg

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