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

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.