microRNA-3607 (miR-3607) has been identified as an important biomarker, and its aberrant expression exerts a significant role in tumorigenesis. However, the biological function of miR-3607 in hepatocellular carcinoma (HCC) needs to be deciphered comprehensively. Clinical samples of HCC patients, as well as normal cases, were derived from The Cancer Genome Atlas database. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting analyses were utilized to detect the expression levels of indicated genes. Cell counting kit-8 (CCK-8), colony formation, and transwell assays were performed to assess the effect of miR-3607 in HCC cell viability, migration, and invasion. Bioinformatics analysis and luciferase reporter gene assay was applied to screen the target genes of miR-3607 and verified the association between miR-3607 and its potential target gene. Our study showed that miR-3607 expression was decreased in HCC tissues and cell lines, and its downregulation was linked with poor outcomes of HCC patients. miR-3607 was noted to inhibit HCC cell growth, colony formation, migration, and invasion. Besides, minichromosome maintenance (MCM5) was a possible target gene of miR-3607 in HCC. Overexpression of MCM5 was observed in HCC and induced unfavorable prognosis. MCM5 expression had a negative correlation with miR-3607. MCM5 can abolish the suppressive impacts of miR-3607 on HCC cell malignant behaviors and the epithelial-mesenchymal transition (EMT) process. To sum up, our results unveiled that miR-3607 could inhibit HCC cell growth, migration, and invasion by regulating MCM5 and mediating EMT process, suggesting a new probable biomarker for further treatment of HCC.
Keywords: EMT; MCM5; hepatocellular carcinoma; miR-3607; prognosis.
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