MicroRNA‑758 inhibits cervical cancer cell proliferation and metastasis by targeting HMGB3 through the WNT/β‑catenin signaling pathway
- Authors:
- Published online on: June 12, 2019 https://doi.org/10.3892/ol.2019.10470
- Pages: 1786-1792
-
Copyright: © Song et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Metrics: Total
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
Abstract
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.
