LncRNA RP11-89 facilitates tumorigenesis and ferroptosis resistance through PROM2-activated iron export by sponging miR-129-5p in bladder cancer

Male Carcinogenesis Iron Mice, Nude Article Cohort Studies 03 medical and health sciences Cell Line, Tumor Animals Ferroptosis Humans Aged Mice, Inbred BALB C 0303 health sciences Binding Sites Membrane Glycoproteins QH573-671 Base Sequence Biological Transport Cell Cycle Checkpoints 3. Good health Gene Expression Regulation, Neoplastic MicroRNAs Ferritins Female Cytology
DOI: 10.1038/s41419-021-04296-1 Publication Date: 2021-11-02T08:02:48Z
ABSTRACT
Abstract Long non-coding RNAs (lncRNAs) act as important regulators of tumorigenesis and development in bladder cancer. However, the underlying molecular mechanisms remain elusive. We previously identified a novel lncRNA signature related to immunity progression Here we further explored function RP11-89, discovered previous signature. Loss- gain-of experiments were performed using CCK-8 assay, flow cytometry, Transwell assays, scratch tests subcutaneous nude mouse models. High-throughput RNA sequencing was conducted identify dysregulated genes cancer cells with RP11-89 knockdown or overexpression. Regulation on miR-129-5p PROM2 through luciferase reporter RIP assay pull-down assay. promoted cell proliferation, migration inhibited cycle arrest via miR-129-5p/PROM2 axis. found that “sponges” upregulates PROM2. Elevated associated attenuated ferroptosis iron export, formation multivesicular bodies less mitochondrial abnormalities. demonstrated is tumorigenic regulator inhibits PROM2-activated export. may serve potential biomarker for targeted therapy
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