miR‑142‑3p reduces the viability of human cervical cancer cells by negatively regulating the cytoplasmic localization of HMGB1
Affiliations: Department of Obstetrics, Tianjin Central Hospital of Gynecology and Obstetrics, Tianjin 300052, P.R. China, Department of Gynecology, Tianjin Central Hospital of Gynecology and Obstetrics, Tianjin 300052, P.R. China
- Published online on: January 14, 2021 https://doi.org/10.3892/etm.2021.9644
Copyright: © Dong
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High mobility group protein B1 (HMGB1) is a nuclear protein that has been reported to contribute to tumor growth in humans. The present study identified a microRNA (miR/miRNA) that targets the 3' untranslated region (3'UTR) of the HMGB1 gene and assessed its effects on the proliferation of human cervical cancer cells and associated molecular mechanism. Western blotting was performed to determine HMGB1 levels in HeLa cells. TargetScan software was used to identify miRNA binding sites adjacent to the HMGB1. The viability of HeLa cells transfected with miR‑142‑3p mimics or inhibitors was determined using an MTT assay. The subcellular distribution (cytoplasmic or nuclear) of HMGB1 in HeLa cells was observed by western blotting. HMGB1 expression in HeLa and CaSKi cells was significantly higher compared with normal control cervical cells. TargetScan analysis indicated that miR‑142‑3p binds to the 3'UTR of HMGB1. Transfection with a miR‑142‑3p inhibitor increased cytoplasmic HMGB1 expression in HeLa cells, as shown by western blot analysis, while transfection with miR‑142‑3p mimics decreased the cytoplasmic expression of HMGB1 in HeLa cells. Therefore, miR‑142‑3p negatively regulated HMGB1 levels in cervical cancer cells. These findings indicated that miR‑142‑3p inhibited the proliferation of human cervical cancer cells, at least in part, by negatively regulating the cytoplasmic localization of HMGB1.