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首页> 外文期刊>Journal of Cellular Physiology >MicroRNA‐497 accelerates apoptosis while inhibiting proliferation, migration, and invasion through negative regulation of the MAPK/ERK signaling pathway via RAF‐1
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MicroRNA‐497 accelerates apoptosis while inhibiting proliferation, migration, and invasion through negative regulation of the MAPK/ERK signaling pathway via RAF‐1

机译：MicroRNA 497加速细胞凋亡抑制癌细胞增殖、迁移和入侵通过MAPK / ERK的负调控信号通路通过英国皇家空军1

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The aim of this study is to explore the various modes of action miR‐497 has on human cervical cancer (CC) cell behavior. We also speculate that miR‐497 achieves its anti‐tumor role by governing RAF‐1 via MAPK/ERK signaling pathway. CC tissues with corresponding adjacent normal tissues were collected from 168 CC patients. RAF‐1 ‐ positive cells were identified by means of immunohistochemistry in tissues. A series of inhibitors, mimics and siRNA against RAF‐1 were introduced to validate regulatory mechanisms for miR‐497 and RAF‐1. Quantitative real‐time polymerase chain reaction (qRT‐PCR) and Western blot assay were employed for evaluating alternations of miR‐497, RAF‐1, and MAPK/ERK signaling pathway. HeLa cell proliferation, invasion, migration, cycle progression, and apoptosis were assessed by means of CCK‐8, wound‐healing, transwell invasion assays, and flow cytometry, respectively. The target prediction program and luciferase activity determination were used to identify miR‐497 targeting RAF‐1. We determined reduced miR‐497 expression and elevated expression of RAF‐1 in CC tissues as opposed to adjacent tissues. Transfection of miR‐497 mimics and siRNA‐RAF‐1 both decreased levels of MEK1, ERK1, and p38 phosphorylation in HeLa cells, inhibited cell proliferation, migration and invasion, induced more cells arrested in the G0/G1 phase, and promoted cell apoptosis; while miR‐497 inhibitors led to opposite results. These findings indicate miR‐497 as a tumor suppressor results from negative regulation of the MAPK/ERK signaling pathway via RAF‐1 in CC.
机译：本研究的目的是探索不同颈miR量497对人类的行为模式癌症(CC)细胞的行为。米尔量497通过管理来实现其抗肿瘤应承担的角色英国皇家空军1通过MAPK / ERK信号通路。与相应的邻近的正常组织收集的168 CC的病人。细胞被确认通过组织的免疫组织化学。抑制剂,模仿,siRNA反对英国皇家空军1介绍了验证监管机制英国皇家空军(RAF)米尔‐497和‐1。聚合酶链反应(qRT检测PCR)和西方污点分析被用于评估交替的米尔还是497年,英国皇家空军高1和MAPK / ERK信号通路。入侵、移民、循环发展细胞凋亡是评估通过CCK 8,应承担的伤口愈合,应承担transwell入侵检测流式细胞术,分别。预测项目和荧光素酶的活动决心是用来识别miR量497针对空军1。表达和表达升高空军1 CC组织与邻近组织。转染的米尔497模仿和核RAF量1MEK1水平下降,ERK1和p38在海拉细胞磷酸化,抑制细胞增殖、迁移和入侵,诱导更多的细胞在G0 / G1期,被捕促进细胞凋亡;导致相反的结果。米尔497作为一个肿瘤抑制的结果- MAPK / ERK信号调节通过英国皇家空军1 CC应承担的途径。

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