Abstract
Breast cancer (BC) leads to the highest mortality in women worldwide, characterized by inevitable proliferation and metastasis of BC cells. Mounting evidence confirm that lncRNAs play a significant role in the tumorigenesis and development of BC. lncRNA CERS6-AS1 is a novel discovery, and its role and molecular mechanism in BC has not been studied. In this study, it was discovered that CERS6-AS1 was overexpressed in BC tissues and cells. CERS6-AS1 accelerated cell proliferation and suppressed cell apoptosis in BC. Moreover, molecular mechanism exploration uncovered that there was a positive association between CERS6 and CERS6-AS1 (or IGF2BP3) expression in BC. Furthermore, IGF2BP3 serves as a RNA-binding protein for CERS6-AS1 and CERS6-AS1 promoted CERS6 mRNA stability by binding to IGF2BP3. In the end, rescue experiments verified that overexpression of CERS6 rescues the inhibition of CERS6-AS1 deficiency on BC progression in vitro and vivo. Taken together, these evidences suggested that CERS6-AS1 promoted the progression of BC by binding to IGF2BP3 and thus enhancing the stability of CERS6 mRNA, providing a new underlying therapeutic target for BC to improve prognosis.