Exosomes from PYCR1 knockdown bone marrow mesenchymal stem inhibits aerobic glycolysis and the growth of bladder cancer cells via regulation of the EGFR/PI3K/AKT pathway

• DOI: 10.3892/ijo.2023.5532
• Publication Date: 2023-06-09T08:21:41Z
• Authors: Zhuo Li; Ying Jiang; Jian Liu; Huifeng Fu; Quan Yang; Wei Song; Yuanwei Li
• Keywords: Anaerobic glycolysis

Bladder cancer (BC) is a heterogeneous disease, and pyrroline‑5‑carboxylate reductase 1 (PYCR1) can promote the proliferation invasion of BC cells accelerate progression. In present study, si‑PYCR1 was loaded into bone marrow mesenchymal stem cell (BMSC)‑derived exosomes (Exos) in BC. First, PYCR1 levels tissues/cells were assessed, proliferation, invasion, migration evaluated. Aerobic glycolysis (glucose uptake, lactate production, ATP expression relevant enzymes) EGFR/PI3K/AKT pathway phosphorylation determined. PYCR1‑EGFR interactions examined by co‑immunoprecipitation experiments. RT4 transfected with oe‑PYCR1 treated EGFR inhibitor CL‑387785. Exos identified, followed an assessment their effects on aerobic malignant behaviors. Nude mouse models xenograft tumors established injecting mice Exo‑si‑PYCR1 Exo‑si‑PYCR1. upregulated cells, highest observed T24 lowest cells. Following knockdown, behaviors decreased, while overexpression averted these trends. interacted EGFR, CL‑387785 inhibited attenuated but had no effect expression. showed stronger inhibitory than si‑PYCR1. blocked tumor growth good biocompatibility. Briefly, knocking BMSC‑derived suppressed via PI3K/AKT binding to EGFR.