CircRAB3B suppresses proliferation, motility, cell cycle progression and promotes the apoptosis of IL-22-induced keratinocytes depending on the regulation of miR-1228-3p/PTEN axis in psoriasis

Abstract

Abstract Introduction Psoriasis is an immune-related chronic skin disease, and interleukin-22 (IL-22) is involved in psoriasis pathogenesis through promoting proliferation and migration abilities of keratinocytes. Here, we analysed the role of circular RNA (circRNA) RAB3B, member RAS oncogene family (circRAB3B) in regulating the phenotypes of IL-22-induced HaCaT cells. Methods RT-qPCR was implemented to assess RNA abundance. Western blot assay was adopted to assess protein abundance. Cell proliferation capacity was examined by cell counting kit-8 (CCK8) assay and 5-ethynyl-2′-deoxyuridine (Edu) assay. Cell motility was assessed by transwell assays and wound healing assay. Flow cytometric analysis was utilized to evaluate cell cycle progression and apoptosis. The intermolecular binding relations were tested via dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. CircRAB3B expression was reduced in psoriatic cutaneous specimens and IL-22-treated HaCaT cells. Results CircRAB3B overexpression hampered the proliferation, motility, and cell cycle progression and elevated the apoptotic rate of IL-22-treated HaCaT cells, and circRAB3B silencing exhibited opposite effects in IL-22-induced HaCaT cells. CircRAB3B acted as microRNA-1228-3p (miR-1228-3p) sponge in HaCaT cells, and miR-1228-3p overexpression largely overturned circRAB3B overexpression-induced effects in HaCaT cells. MiR-1228-3p interacted with phosphatase and tensin homolog (PTEN), and circRAB3B sponged miR-1228-3p to induce PTEN level. MiR-1228-3p accumulation-mediated effects were partly alleviated by PTEN overexpression in HaCaT cells upon IL-22 treatment. Conclusions CircRAB3B suppressed psoriasis progression partly through down-regulating miR-1228-3p and up-regulating PTEN.