H. Tian, K. Ding, Zhongchao Wang, L. Yin, Jianzhong Wu, Xia He
{"title":"miR‐643 suppresses cell invasion and radioresistant of lung cancer through RAF1","authors":"H. Tian, K. Ding, Zhongchao Wang, L. Yin, Jianzhong Wu, Xia He","doi":"10.1002/prm2.12102","DOIUrl":null,"url":null,"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.","PeriodicalId":40071,"journal":{"name":"Precision Medical Sciences","volume":"12 1","pages":"113 - 120"},"PeriodicalIF":0.4000,"publicationDate":"2023-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Precision Medical Sciences","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/prm2.12102","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
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.