B. Dong, Xiaowei Liu, Suo Wang, Xiujun Chen, Kun Zhang, Ying Zhang
{"title":"微小RNA-125a-5p作为非小细胞肺癌(NSCLC)的肿瘤抑制剂:通过P13K/AKT/MMP信号通路抑制增殖和诱导细胞凋亡","authors":"B. Dong, Xiaowei Liu, Suo Wang, Xiujun Chen, Kun Zhang, Ying Zhang","doi":"10.1166/sam.2023.4457","DOIUrl":null,"url":null,"abstract":"To investigate the effects of micro ribonucleic acid (miR)-125a-5p on the proliferation and apoptosis of non-small cell lung cancer (NSCLC) cells and its possible mechanism. With NSCLC A549 cells as the experimental research objects, transfection reagent was employed to transfect miR-125a-5p\n NC group, miR-125a-5p mimic group and miR-125a-5p siRNA group into A549 cells. qRT-PCR and cloning assays were conducted to detect the level of miR125a-5p in A549 cells and the effect of miR125a-5p on the proliferation of A549 cells. The effect of miR-125a-5p on apoptosis of A549 cells was\n detected via FCM. Additionally, the effects of miR-125a-5p on the mRNA and protein expressions of PI3K and AKT and the expressions of MMP-2 and MMP-9 in A549 cells were determined through qRT-PCR, Western blotting and immunohistochemistry, respectively. Compared with those in miR-125a-5p NC\n group, the proliferation ability of A549 cells was improved, their apoptosis rate was significantly decreased, and the mRNA and protein levels of PI3K and AKT and the levels of MMP-2 and MMP-9 in A549 cells were increased in miR-125a-5p siRNA group, whereas they showed totally opposite tendencies\n in miR-125a-5p mimic group. miR-125a-5p overexpression can hinder A549 cell growth, boost apoptosis, and reduce MMP-2 and MMP-9 levels via the PI3K/AKT/MMP pathway.","PeriodicalId":21671,"journal":{"name":"Science of Advanced Materials","volume":" ","pages":""},"PeriodicalIF":0.9000,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"microRNA-125a-5p as a Tumor Suppressor in Non-Small Cell Lung Cancer (NSCLC): Inhibition of Proliferation and Induction of Apoptosis via P13K/AKT/MMP Signaling Pathway\",\"authors\":\"B. Dong, Xiaowei Liu, Suo Wang, Xiujun Chen, Kun Zhang, Ying Zhang\",\"doi\":\"10.1166/sam.2023.4457\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"To investigate the effects of micro ribonucleic acid (miR)-125a-5p on the proliferation and apoptosis of non-small cell lung cancer (NSCLC) cells and its possible mechanism. With NSCLC A549 cells as the experimental research objects, transfection reagent was employed to transfect miR-125a-5p\\n NC group, miR-125a-5p mimic group and miR-125a-5p siRNA group into A549 cells. qRT-PCR and cloning assays were conducted to detect the level of miR125a-5p in A549 cells and the effect of miR125a-5p on the proliferation of A549 cells. The effect of miR-125a-5p on apoptosis of A549 cells was\\n detected via FCM. Additionally, the effects of miR-125a-5p on the mRNA and protein expressions of PI3K and AKT and the expressions of MMP-2 and MMP-9 in A549 cells were determined through qRT-PCR, Western blotting and immunohistochemistry, respectively. Compared with those in miR-125a-5p NC\\n group, the proliferation ability of A549 cells was improved, their apoptosis rate was significantly decreased, and the mRNA and protein levels of PI3K and AKT and the levels of MMP-2 and MMP-9 in A549 cells were increased in miR-125a-5p siRNA group, whereas they showed totally opposite tendencies\\n in miR-125a-5p mimic group. miR-125a-5p overexpression can hinder A549 cell growth, boost apoptosis, and reduce MMP-2 and MMP-9 levels via the PI3K/AKT/MMP pathway.\",\"PeriodicalId\":21671,\"journal\":{\"name\":\"Science of Advanced Materials\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.9000,\"publicationDate\":\"2023-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Science of Advanced Materials\",\"FirstCategoryId\":\"88\",\"ListUrlMain\":\"https://doi.org/10.1166/sam.2023.4457\",\"RegionNum\":4,\"RegionCategory\":\"材料科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Science of Advanced Materials","FirstCategoryId":"88","ListUrlMain":"https://doi.org/10.1166/sam.2023.4457","RegionNum":4,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
microRNA-125a-5p as a Tumor Suppressor in Non-Small Cell Lung Cancer (NSCLC): Inhibition of Proliferation and Induction of Apoptosis via P13K/AKT/MMP Signaling Pathway
To investigate the effects of micro ribonucleic acid (miR)-125a-5p on the proliferation and apoptosis of non-small cell lung cancer (NSCLC) cells and its possible mechanism. With NSCLC A549 cells as the experimental research objects, transfection reagent was employed to transfect miR-125a-5p
NC group, miR-125a-5p mimic group and miR-125a-5p siRNA group into A549 cells. qRT-PCR and cloning assays were conducted to detect the level of miR125a-5p in A549 cells and the effect of miR125a-5p on the proliferation of A549 cells. The effect of miR-125a-5p on apoptosis of A549 cells was
detected via FCM. Additionally, the effects of miR-125a-5p on the mRNA and protein expressions of PI3K and AKT and the expressions of MMP-2 and MMP-9 in A549 cells were determined through qRT-PCR, Western blotting and immunohistochemistry, respectively. Compared with those in miR-125a-5p NC
group, the proliferation ability of A549 cells was improved, their apoptosis rate was significantly decreased, and the mRNA and protein levels of PI3K and AKT and the levels of MMP-2 and MMP-9 in A549 cells were increased in miR-125a-5p siRNA group, whereas they showed totally opposite tendencies
in miR-125a-5p mimic group. miR-125a-5p overexpression can hinder A549 cell growth, boost apoptosis, and reduce MMP-2 and MMP-9 levels via the PI3K/AKT/MMP pathway.