MicroRNA‑485 targets MACC1 and inhibits cervical cancer cell proliferation and invasion.

A large body of evidence has indicated that microRNAs (miRNAs/miRs) have essential roles in the development and progression of cervical cancer. Thus, miRNAs with dysregulated expression are potential biomarkers for cervical cancer diagnosis and prognosis. In the present study, expression levels of miR‑485 were detected in cervical cancer tissues and cell lines. The effects of miR‑485 overexpression on the proliferation and invasion of cervical cancer cells were determined with Cell Counting kit‑8 and Transwell invasion assays. The mechanisms underlying the action of miR‑485 in cervical cancer were investigated using bioinformatics analysis, a luciferase reporter assay, reverse transcription‑quantitative polymerase chain reaction and western blot analysis. In addition, the association between miR‑485 and metastasis associated in colon cancer‑1 (MACC1) in cervical cancer tissues was examined. The present study demonstrated that miR‑485 expression was significantly downregulated in cervical cancer tissues and cell lines. Reduced miR‑485 expression in patients with cervical cancer was correlated with International Federation of Gynecology and Obstetrics stage and lymph node metastasis. Furthermore, restored expression of miR‑485 significantly reduced cervical cancer cell proliferation and invasion. MACC1 was identified as a direct target gene of miR‑485 in cervical cancer. MACC1 expression was significantly upregulated in cervical cancer specimens and was inversely correlated with miR‑485 expression. Additionally, the restored expression of MACC1 eliminated the suppressive effects of miR‑485 overexpression on the proliferation and invasion of cervical cancer cells. Notably, the upregulation of miR‑485 suppressed the MET proto‑oncogene, receptor tyrosine kinase (Met)/RAC‑α serine/threonine‑protein kinase (AKT) signaling pathway. These results demonstrated that miR‑485 may perform its tumor suppressive function in cervical cancer by directly targeting MACC1 and inhibiting the Met/AKT signaling pathway. Therefore, the miR‑485/MACC1 axis may be a novel and effective therapeutic target in cervical cancer.