Isoflurane enhances the expression of circ_0088233 to promote the malignancy of prostate cancer through circ_0088233-mediated miR-33b-5p/HIF1A pathway

Abstract Background The effects of isoflurane (Iso) on the viability and migration of cancer cells is crucial for the use of Iso in tumor resection. The objective of this study was to evaluate the effect of Iso on the function of prostate cancer (PCa) in cell proliferation, survival and migration, and to explore the potential mechanism of isoflurane action from the perspective of circular RNA (circRNA). Methods The effects of Iso on cell viability, cell apoptosis, cell invasion and cell migration were determined by cell counting kit-8 (CCK-8), flow cytometry, transwell and wound healing assays, respectively. The expression of circ_0088233, microRNA-33b-5p (miR-33b-5p) and hypoxia inducible factor 1 subunit alpha (HIF1A) was detected by quantitative real-time PCR (qPCR). The underlying relationship between miR-33b-5p and circ_0088233 or HIF1A was verified by dual-luciferase reporter assay and RNA pull-down assay. Animal study was conducted to determine the effects of Iso in vivo. Results Iso enhanced PCa cell viability, invasion and migration and inhibited cell apoptosis. Iso promoted the expression of circ_0088233, and circ_0088233 knockdown partly abolished the effects of Iso and thus inhibited PCa cell malignant behaviors. MiR-33b-5p was a target of circ_0088233, and HIF1A was a target of miR-33b-5p. Circ_0088233 knockdown inhibited PCa cell malignant behaviors by enriching miR-33b-5p, and miR-33b-5p restoration inhibited PCa cell malignant behaviors by sequestering HIF1A. Iso contributed to tumor growth in vivo by increasing circ_0088233 expression. Conclusion Iso strengthened the expression of circ_0088233 to promote the malignant development of PCa through circ_0088233-mediated miR-33b-5p/HIF1A pathway.