LncRNA Phosphatase and Tensin Homolog Induced Kinase 1-AS Promotes Insulin Like Growth Factor 1 Receptor Expression Through Sponge miR-98-5p and Contributes to Bladder Cancer Progression
{"title":"LncRNA Phosphatase and Tensin Homolog Induced Kinase 1-AS Promotes Insulin Like Growth Factor 1 Receptor Expression Through Sponge miR-98-5p and Contributes to Bladder Cancer Progression","authors":"Shunping Wang, DanPing Cheng, Bin Zheng","doi":"10.1166/jbt.2023.3259","DOIUrl":null,"url":null,"abstract":"Background: LncRNA PINK1-AS is an identified key modifier in cancers, but its biological function in bladder cancer (BC) remains unclear. The current work tried to explore the function and mechanism of PINK1-AS in BC. Methods: Fifty-five pairs of BC tissue and matched\n para-cancer normal tissue were excised to analyze PINK1-AS, miR-98-5p, and IGF1R expression. Based on T24 cells, the proliferative, apoptotic, invasive, and migratory activities were evaluated by CCK-8, flow cytometry, and Transwell assay correspondingly. RIP and dual luciferase reporter assays\n verified binding relationships between genes. Results: PINK1-AS expression was abnormally high in BC tissues, and was associated with TNM staging and lymph node metastasis in BC patients. PINK1-AS knockdown delayed the malignant progression in BC. Overexpressing PINK1-AS had the opposite\n effect. The impacts of silencing or promoting PINK1-AS on BC were mitigated by overexpression of IGF1R and miR-98-5p, respectively. PINK1-AS was competitively bound to miR-98-5p to mediate IGF1R expression. Conclusion: Targeting the abnormally overexpressed lncRNA, PINK1-AS, can release\n the inhibition of IGF1R by miR-98-5p, thereby promoting BC malignancy. PINK1-AS/miR-98-5p/IGF1R axis can be used as a potential therapeutic target for BC.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1000,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biomaterials and Tissue Engineering","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1166/jbt.2023.3259","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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Abstract
Background: LncRNA PINK1-AS is an identified key modifier in cancers, but its biological function in bladder cancer (BC) remains unclear. The current work tried to explore the function and mechanism of PINK1-AS in BC. Methods: Fifty-five pairs of BC tissue and matched
para-cancer normal tissue were excised to analyze PINK1-AS, miR-98-5p, and IGF1R expression. Based on T24 cells, the proliferative, apoptotic, invasive, and migratory activities were evaluated by CCK-8, flow cytometry, and Transwell assay correspondingly. RIP and dual luciferase reporter assays
verified binding relationships between genes. Results: PINK1-AS expression was abnormally high in BC tissues, and was associated with TNM staging and lymph node metastasis in BC patients. PINK1-AS knockdown delayed the malignant progression in BC. Overexpressing PINK1-AS had the opposite
effect. The impacts of silencing or promoting PINK1-AS on BC were mitigated by overexpression of IGF1R and miR-98-5p, respectively. PINK1-AS was competitively bound to miR-98-5p to mediate IGF1R expression. Conclusion: Targeting the abnormally overexpressed lncRNA, PINK1-AS, can release
the inhibition of IGF1R by miR-98-5p, thereby promoting BC malignancy. PINK1-AS/miR-98-5p/IGF1R axis can be used as a potential therapeutic target for BC.