Department of Nuclear Medicine, The Second Hospital of Jilin University, Changchun, China.
Department of Dermatology, The Second Hospital of Jilin University, Changchun, China.
Gynecol Obstet Invest. 2021;86(1-2):71-80. doi: 10.1159/000511771. Epub 2020 Dec 1.
The objective of this study is to explore the role of miR-210 in the growth of ovarian cancer cells and the correlation with radiotherapy and to elucidate underlying molecular mechanisms.
Human ovarian cancer cell lines OVCAR3 and SKOV3 were cultured in vitro, and miR-210 over-expression and low-expression ovarian cancer cell models were established by cell transfection. MTT assay was used to detect the proliferation activity. Transwell was used to detect the migration and invasion abilities. Western blot measured the expression of proteins related to cell proliferation, migration, and invasion. The cells were treated with different doses of ionizing radiation, and then the cell proliferation activity was detected by MTT. The expression of apoptosis-related proteins was detected by Western blot. The Caspase-Glo® Kit was used to detect the activity of cellular caspase 3/7 enzymes.
The proliferation, migration, and invasion abilities of miR-210 over-expression ovarian cancer cells were increased (p < 0.05), the expressions of PTEN and E-cadherin were decreased, and the expression of p-Protein kinase B (AKT), N-cadherin, Snail, and Vimentin were elevated. After ionizing radiation, the sensitivity of miR-210 over-expression cells to radiotherapy was decreased, the expression of apoptosis-related protein Bax was decreased, the expression of Bcl-2 was increased, and the activity of cellular caspase 3/7 enzyme was reduced (p < 0.05).
miR-210 can promote the proliferation, migration, and invasion of ovarian cancer cells by activating the AKT signaling pathway and regulating the expression of Epithelial-mesenchymal transition-related proteins. miR-210 can reduce the sensitivity of ovarian cancer cells to radiotherapy by inhibiting apoptosis, which might serve as a potential target for the treatment of ovarian tumors.
本研究旨在探讨 miR-210 在卵巢癌细胞生长中的作用及其与放疗的相关性，并阐明其潜在的分子机制。
体外培养人卵巢癌细胞系 OVCAR3 和 SKOV3，通过细胞转染构建 miR-210 过表达和低表达卵巢癌细胞模型。MTT 法检测细胞增殖活性。Transwell 法检测细胞迁移和侵袭能力。Western blot 检测与细胞增殖、迁移和侵袭相关的蛋白表达。用不同剂量电离辐射处理细胞，MTT 法检测细胞增殖活性。Western blot 检测细胞凋亡相关蛋白表达。Caspase-Glo® Kit 检测细胞内 caspase 3/7 酶的活性。
miR-210 过表达卵巢癌细胞的增殖、迁移和侵袭能力增强（p<0.05），PTEN 和 E-cadherin 的表达降低，p-蛋白激酶 B（AKT）、N-cadherin、Snail 和 Vimentin 的表达升高。经电离辐射处理后，miR-210 过表达细胞对放疗的敏感性降低，凋亡相关蛋白 Bax 的表达降低，Bcl-2 的表达升高，细胞内 caspase 3/7 酶的活性降低（p<0.05）。
miR-210 可通过激活 AKT 信号通路和调节上皮间质转化相关蛋白的表达促进卵巢癌细胞的增殖、迁移和侵袭。miR-210 可通过抑制细胞凋亡降低卵巢癌细胞对放疗的敏感性，可能成为卵巢肿瘤治疗的潜在靶点。
