CircSETD2 inhibits YAP1 by interaction with HuR during breast cancer progression.

CircRNAs have been proven to play a pivotal role in cancer progression. The present study aims to explore the roles and related mechanisms of circSETD2 in breast cancer proliferation, migration and invasion. The expression of circSETD2 in BC was assessed by the GEO database and qRT‒PCR. The biological function and underlying molecular mechanism of circSETD2 in BC were explored using in vitro and in vivo experiments, including CCK8, transwell, RIP, western blot, and xenograft mouse models. The expression of circSETD2 was downregulated in BC tumors, in accordance with the GEO database. Overexpression of circSETD2 significantly suppressed cell growth, cell migration and invasion. Mechanistically, circSETD2 reduced the stabilization of YAP1 by competitively binding with HuR, resulting in inactivation of downstream targets such as CTGF, myc and Slug. Our work suggests that the novel signaling axis circSETD2/HuR/YAP1 plays an important role in BC progression. The molecular mechanism underlying this signaling axis may provide a potential therapeutic target for BC treatment.