miR-141-5p positively regulates ACVRL1 expression to promote cervical cancer progression.

Global cancer data show a continuous rise in cervical cancer incidence and mortality, burdening public health. To effectively mitigate this challenge, elucidating molecular pathogenesis and novel drug targets are critical for advancing clinical care. In this study, abnormally expressed miRNAs in cervical cancer were identified through TCGA data analysis. Expression levels were quantified using qRT-PCR and Western Blot, at both mRNA and protein levels, respectively. miR-141-5p and ACVRL1's interaction was validated with dual-luciferase assays. Cell behavior was evaluated using assays including CCK-8 assay. In vivo tumor growth was assessed in nude mice xenograft model. Database screening and subsequent validation using cancer cell lines and clinical samples revealed aberrantly elevated expression of miR-141-5p in cervical cancer. High expression of miR-141-5p in SiHa/HeLa cells significantly promoted cellular proliferation, migration, and invasion while concurrently inhibiting apoptosis, whereas its downregulation elicited opposing effects. ACVRL1 was identified as a direct target of miR-141-5p. Overexpressing miR-141-5p markedly upregulated ACVRL1 mRNA and protein levels, while its knockdown significantly reduced ACVRL1 expression at both mRNA and protein levels. Further functional analysis showed that ACVRL1 knockdown significantly impaired cellular proliferation, migration, and invasion while enhancing apoptosis in cervical cancer cells. Rescue experiments confirmed that miR-141-5p exerted regulatory effects on these cellular behaviors, at least partially through ACVRL1. miR-141-5p downregulation significantly suppressed tumor growth in vivo, as evidenced by reduced tumor volume and weight in nude mice. In brief, this study shows that miR-141-5p upregulation in cervical cancer promotes tumor progression via ACVRL1 regulation, indicating its potential in precision oncology.