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Reduced levels of miR‐485‐5p in HPV‐infected cervical cancer promote cell proliferation and enhance invasion ability

Cervical cancer (CC) is the most common gynecological malignancy, with high incidence and mortality rates in China. The microRNA miR‐485‐5p has previously been reported to serve as a negative regulator of tumorigenesis in breast cancer and hepatocellular carcinoma, and miR‐485‐5p has been observed t...

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Detalles Bibliográficos
Autores principales: Dai, Yuanyuan, Xie, Fengyan, Chen, Yan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7327903/
https://www.ncbi.nlm.nih.gov/pubmed/32343879
http://dx.doi.org/10.1002/2211-5463.12869
Descripción
Sumario:Cervical cancer (CC) is the most common gynecological malignancy, with high incidence and mortality rates in China. The microRNA miR‐485‐5p has previously been reported to serve as a negative regulator of tumorigenesis in breast cancer and hepatocellular carcinoma, and miR‐485‐5p has been observed to be differentially expressed between CC and normal control tissue. Here, we confirmed that miR‐485‐5p expression is lower in CC than in adjacent normal tissue and proceeded to investigate the effects of miR‐485 on tumor behavior in CC cell lines. We report that miR‐485‐5p transcription is decreased in HPV‐infected CC tissue, and levels of miR‐485 in clinical samples are positively correlated with the 5‐year overall survival rate. The Transwell assay showed that miR‐485‐5p inhibited cell invasion and migration but had no influence on apoptosis and cell proliferation. Using a luciferase reporter assay, we demonstrated that miR‐485‐5p partially abrogated cell migration and proliferation by targeting FLOT‐1 mRNA. Transfection of HPV‐infected cervical carcinoma cells with an adenovirus vector encoding human FLOT‐1 partially diminished the inhibitory effects of miR‐485 on cell invasion. Taken, together, these data demonstrated that miR‐485‐5p suppresses the invasion of cancer cells by targeting FLOT‐1 in HPV‐infected cervical carcinoma cells.