CircOAS3 Regulates Keratinocyte Proliferation and Psoriatic Inflammation by Interacting with Hsc70 via the JNK/STAT3/NF-κB Signaling Pathway.

Psoriasis is a chronic inflammatory disease of the skin with a very complex pathogenesis. Circular RNAs (circRNAs) play important regulatory roles in many diseases, including psoriasis. In this study, we found that circOAS3 expression was significantly upregulated in both psoriatic tissues and M5-induced keratinocytes. Silencing circOAS3 in HaCaT and Ker-CT cells inhibited their viability, promoted apoptosis, and blocked the cell cycle from the G1 to the S phase. RNA pull-down and RNA immunoprecipitation (RIP) analyses led to the identification of a direct interaction between circOAS3 and heat shock cognate protein 70 (Hsc70). Silencing circOAS3 expression negatively influenced Hsc70 protein expression but not mRNA expression. circOAS3 knockdown suppressed the activation of the JNK/STAT3/NF-κB signaling pathway. circOAS3 or Hsc70 silencing led to downregulated protein IL-6 expression, thus reducing psoriatic inflammation in vitro. In conclusion, the interaction between circOAS3 and Hsc70 mediates the proliferation and psoriatic inflammation of HaCaT and Ker-CT cells through the JNK/STAT3/NF-κB signaling pathway, suggesting that circOAS3 or Hsc70 may be a promising therapeutic target for psoriasis.