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miR-3188 Regulates Cell Proliferation, Apoptosis, and Migration in Breast Cancer by Targeting TUSC5 and Regulating the p38 MAPK Signaling Pathway

机译:MiR-3188通过靶向TUSC5并调节P38 MAPK信号通路来调节乳腺癌细胞增殖,细胞凋亡和迁移

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This study intended to investigate the effects of miR-3188 on breast cancer and to reveal the possible molecular mechanisms. miR-3188 was upregulated and TUSC5 was downregulated in breast cancer tissues and MCF-7 cells compared to normal tissue and MCF-10 cells. After MCF-7 cells were transfected with miR-3188 inhibitor. cell proliferation and migration were inhibited, whereas apoptosis was promoted. Luciferase reporter assay suggested that TUSC5 was a target gene of miR-3188. In addition, miR-3188 overexpression increased the p-p38 expression, while miR-3188 suppression decreased the p-p38 expression significantly. miR-3188 regulated breast cancer progression via the p38 MAPK signaling pathway. In conclusion. miR-3188 affects breast cancer cell proliferation, apoptosis, and migration by targeting TUSC5 and activating the p38 MAPK signaling pathway. miR-3188 may serve as a potential therapeutic agent for the treatment of breast cancer.
机译:该研究旨在探讨miR-3188对乳腺癌的影响,揭示可能的分子机制。 与正常组织和MCF-10细胞相比,MiR-3188被上调,并且TUSC5在乳腺癌组织和MCF-7细胞中下调。 用miR-3188抑制剂转染MCF-7细胞后。 抑制细胞增殖和迁移,而促进细胞凋亡。 荧光素酶报告结果表明TUSC5是miR-3188的靶基因。 此外,miR-3188过表达增加了p-p38表达,而miR-3188抑制显着降低了p-p38表达。 MiR-3188通过P38 MAPK信号通路调节乳腺癌进展。 综上所述。 MiR-3188通过靶向TUSC5并激活P38 MAPK信号通路来影响乳腺癌细胞增殖,细胞凋亡和迁移。 miR-3188可以用作治疗乳腺癌的潜在治疗剂。

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