Cervical cancer (CC) remains a highly prevalent cancer and cause of mortality amongst women worldwide. miR-758 has been demonstrated to be associated with tumorigenesis by controlling the expression of oncogenic or tumor suppressor genes. However, the function and mechanisms of miR-758 in CC have not been well illustrated. The present study aimed to dissect the effect of miR-758 on the proliferation, migration and invasion of CC cells and determine the potential underlying molecular mechanism of these effects. qPCR results revealed that the expression of miR-758 was significantly decreased in CC tissues and cell lines compared with that in normal tissues and normal cells. Results of CCK-8, colony formation and Transwell assays revealed that miR-758 overexpression markedly decreased cell viability, proliferation, invasion and migration. However, miR-758 inhibitors significantly increased viability, proliferation, invasion and migration. In the mechanism study, we demonstrated that high mobility group box 3 (HMGB3) was a direct target of miR-758, and HMGB3 overexpression rescued the viability, proliferation, invasion and migration of HeLa cells reduced by an miR-758 mimic. It was demonstrated that HMGB3 regulated the WNT/β-catenin signaling pathway under miR-758 regulation. In summary, these observations suggested that miR-758 is a tumor suppressor gene that can inhibit the metastatic phenotype of CC cells by negatively regulating HMGB3, which may present a path to novel therapeutic stratagems for CC therapy.
Keywords: HMGB3; WNT/β-catenin signaling pathway; cervical cancer; microRNA-758; migration and invasion; proliferation.