Effects and mechanisms of lncRNA PTENP1 on proliferation, apoptosis, migration, and invasion of bladder cancer cells by regulating SCARA5 expression
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Abstract:
[Abstract] Objective: To investigate the functional mechanism of bone marrow mesenchymal stem cell (BMSC)-derived exosome lncRNA PTENP1 in bladder cancer progression. Methods: Exosomes from BMSC (BMSC-Exo) were characterized using transmission electron microscopy, nanoparticle tracking analysis (NTA), and WB assay for exosomal markers. The uptake of exosomes derived from BMSC by bladder cancer 5637 cells was confirmed through confocal microscopy. Based on different transfectants, bladder cancer cells (5637 and T24) were divided into groups: control group (no exosomes), BMSC-Exo group, BMSC OE-NC-Exo group, BMSC OE-PTENP1-Exo group, BMSC sh-NC-Exo group, and BMSC sh-PTENP1-Exo group, and co-cultured with respective exosomes (20 μg/mL). The evaluation of cell proliferation, apoptosis, migration, and invasion was conducted using CCK-8, colony formation, flow cytometry, wound healing, and Transwell assays, respectively. The interactions involving miR-17 with PTENP1 and scavenger receptor class A member 5 (SCARA5) were validated using dual luciferase reporter assays, RNA pull-down, and RNA immunoprecipitation (RIP) methods. Results: qRT-PCR showed that BMSC exosomes overexpressing PTENP1 (BMSC OE-PTENP1 Exo) significantly elevated PTENP1 levels in bladder cancer cells (P < 0.01). BMSC OE-PTENP1-Exo inhibited cell proliferation (P < 0.01), migration (P < 0.01), and invasion (P < 0.01), and promoted cell apoptosis (P < 0.01). Furthermore, in vivo experiments showed that BMSC OE-PTENP1-Exo significantly inhibited tumor growth in nude mice (P < 0.01). Conclusion: BMSC-derived exosomal PTENP1 inhibits BC progression by upregulating the expression of SCARA5 via sponging miR-17, providing a potential new therapeutic target for bladder cancer bladder cancer treatment.