ELAVL1 overexpression potentiates cervical cancer malignancy via regulating the ACVRL1/CASP14 pathway

Cervical cancer is the fourth common gynecological malignancy. To explore new therapeutic targets, we found that the transcriptional and translational levels of ELAVL1 were markedly increased in SiHa and HeLa cells as well as cervical cancer specimens. Knockdown of ELAVL1 substantially suppressed the proliferation, invasion, and migration of cervical cancer cells, while inducing apoptosis. Conversely, overexpression of ELAVL1 resulted in a substantial increase in the proliferative, invasive, and migratory capacities of SiHa cells. Bioinformatics predictions, RIP-qPCR and dual-luciferase reporter assays indicated that ELAVL1 might interact with the 3'UTR of ACVRL1, and upregulate ACVRL1 and CASP14 expression. Co-transfection experiments and functional assays revealed that ELAVL1 might modulate malignant phenotypes of cervical cancer cells via the ACVRL1/CASP14 pathway. Furthermore, in vivo si-ELAVL1 administration significantly inhibited tumor growth in nude mouse xenograft models. ELAVL1 may promote cervical cancer progression, potentially through regulating the ACVRL1/CASP14 pathway, rendering ELAVL1 a potential candidate for therapeutic intervention.