miR-152-3p facilitates cell adhesion and hepatic metastases in colorectal cancer via targeting AQP11

Background: Tumor metastasis is a fundamental reason for the poor prognosis of colorectal cancer (CRC) patients. Publications suggested that upregulated Aquaporin-11 (AQP11) can improve CRC patients' prognoses, but few articles investigated the regulation of AQP11 in CRC cell adhesion and hepatic metastases. Therefore, this study will explore the regulatory mechanism of AQP11 regulating CRC cell adhesion and hepatic metastases at the molecular level. Methods: AQP11 and miR-152-3p expression were analyzed based on The Cancer Genome Atlas-Colon Adeno-carcinoma/Rectum Adenocarcinoma (TCGA-COAD/READ) dataset and several other datasets. The upstream genes of AQP11 were predicted via StarBase and MicroRNA Data Integration Portal (mirDIP) databases. The signaling pathways in which the downregulated AQP11 enriched were analyzed via Gene Set Enrichment Analysis (GSEA). Cell proliferation, migration, invasion, and adhesion were respectively tested via western blot, Transwell, and cell adhesion assays. The expression of adhesion-related proteins was determined via enzyme -linked immunosorbent assay (ELISA). AQP11 protein level was examined via western blot, and AQP11 func-tions were validated via nude mice xenograft experiment. Results: AQP11 was downregulated in CRC, and the upregulated AQP11 remarkably repressed cell proliferation, migration, invasion, and adhesion. The silenced AQP11 notably facilitated the above cell functions in CRC. In addition, AQP11 was negatively regulated by miR-152-3p. In vitro cellular assays revealed that miR-152-3p, by targeting AQP11, facilitated CRC cell proliferation, migration, invasion, and adhesion. An in vivo assay suggested that AQP11 could notably repress CRC growth and metastasis. Conclusion: The above results confirmed that miR-152-3p/AQP11 axis could regulate CRC hepatic metastases and would be a promising target in anti-cancer treatment.