miR‐643 suppresses cell invasion and radioresistant of lung cancer through RAF1

IF 0.4 Q4 MEDICINE, RESEARCH & EXPERIMENTAL
H. Tian, K. Ding, Zhongchao Wang, L. Yin, Jianzhong Wu, Xia He
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引用次数: 0

Abstract

RAF1 (c‐raf) has been known as an important tumor‐promoter in many cancers. However, the regulatory mechanisms affecting RAF1 expressions are rarely reported. This study aimed to predict the candidate miRNAs of RAF1 gene and verify their functions in the progression of lung cancer. The expression of miR‐643 was detected by reverse transcription polymerase chain reaction (RT‐PCR). A dual‐luciferase report system was used to verify the relationship between miR‐643 and RAF1. RT‐PCR and Western blot were used to analyze the regulatory relationship between miR‐643 and RAF1. Transwell chamber, scratch, and monoclonal tests showed that miR‐643 affected the proliferation, migration, and radiosensitivity of H1299 and A549 cells by targeting the RAF1 gene. The expression of miR‐643 in lung cancer cells was lower than that in the bronchial epithelioid cells (CRL‐2741), and luciferase reporter experiment confirmed that miR‐643 targeted RAF1. MiR‐643 overexpression decreased the RAF1 expression, thereby decreasing cell migration, proliferation, and radiation resistance through the AKT/nuclear factor‐κB pathway. miR‐643 in lung cancer cells could inhibit cell proliferation, invasion, and metastasis and increase the radiosensitivity by downregulating RAF1.
miR - 643通过RAF1抑制肺癌细胞侵袭和放射耐药
RAF1 (c‐raf)在许多癌症中被认为是一个重要的肿瘤启动子。然而,影响RAF1表达的调控机制鲜有报道。本研究旨在预测RAF1基因的候选mirna,并验证其在肺癌进展中的功能。逆转录聚合酶链反应(RT‐PCR)检测miR‐643的表达。双荧光素酶报告系统用于验证miR - 643和RAF1之间的关系。RT‐PCR和Western blot分析miR‐643与RAF1的调控关系。Transwell chamber、scratch和单克隆实验表明,miR‐643通过靶向RAF1基因影响H1299和A549细胞的增殖、迁移和放射敏感性。miR‐643在肺癌细胞中的表达低于支气管上皮样细胞(CRL‐2741),荧光素酶报告基因实验证实miR‐643靶向RAF1。MiR - 643过表达降低了RAF1的表达,从而通过AKT/核因子κB途径降低了细胞的迁移、增殖和辐射抗性。miR - 643在肺癌细胞中通过下调RAF1表达抑制细胞增殖、侵袭和转移,增加放射敏感性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Precision Medical Sciences
Precision Medical Sciences MEDICINE, RESEARCH & EXPERIMENTAL-
自引率
0.00%
发文量
33
审稿时长
15 weeks
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