Literature DB >> 28927151

MicroRNA-320 suppresses cervical cancer cell viability, migration and invasion via directly targeting FOXM1.

Can Shi1, Zhenyu Zhang1.   

Abstract

Cervical cancer is one of the most common types of gynecological cancer worldwide. MicroRNA-320 (miR-320) has been reported to be downregulated in a number of types of human cancer. However, the expression level and functions of miR-320 in cervical cancer remain unknown. In the present study, miR-320 was identified to be markedly downregulated in cervical cancer tissues and cell lines. For the functional studies, miR-320 mimic or miR-320 inhibitor was introduced into cervical cancer cell lines. The effects of miR-320 on cervical cancer cell viability, migration and invasion were evaluated using MTT, migration and invasion assays, respectively. The results of the present study identified that overexpression of miR-320 suppressed the viability, migration and invasion of cervical cancer cells. In contrast, underexpression of miR-320 improved the viability, migration and invasion of cervical cancer cells. Bioinformatics analysis, dual-luciferase reporter assay and western blot analysis were adopted to investigate the underlying molecular mechanism of the suppressive functions of miR-320 in cervical cancer. The results of the present study demonstrated that miR-320 negatively regulated forkhead box M1 (FOXM1) expression by directly targeting the 3' untranslated region of FOXM1. Furthermore, the functions of FOXM1 short interfering RNA were similar to those induced by miR-320 in cervical cancer, identifying FOXM1 as a functional target of miR-320 in cervical cancer. The results of the present study indicated that miR-320 acted as a tumor suppressor in the viability, migration and invasion of cervical cancer through directly targeting FOXM1, suggesting that miR-320 may be a target for the therapeutic treatment of cervical cancer.

Entities:  

Keywords:  cervical cancer; forkhead box M1; metastasis; microRNA-320; prognosis

Year:  2017        PMID: 28927151      PMCID: PMC5588065          DOI: 10.3892/ol.2017.6647

Source DB:  PubMed          Journal:  Oncol Lett        ISSN: 1792-1074            Impact factor:   2.967


  36 in total

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