miR‑210 regulates esophageal cancer cell proliferation by inducing G2/M phase cell cycle arrest through targeting PLK1

Li,Chenglin; Zhou,Xinliang; Wang,Yadi; Jing,Shaowu; Yang,Congrong; Sun,Guogui; Liu,Qing; Cheng,Yunjie; Wang,Lan

doi:10.3892/mmr.2014.2416

miR‑210 regulates esophageal cancer cell proliferation by inducing G2/M phase cell cycle arrest through targeting PLK1

Authors:
- Chenglin Li
- Xinliang Zhou
- Yadi Wang
- Shaowu Jing
- Congrong Yang
- Guogui Sun
- Qing Liu
- Yunjie Cheng
- Lan Wang
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Affiliations: Department of Radiation Oncology, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, P.R. China, Department of Oncology, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, P.R. China, Department of Oncology, The People's Hospital of Tangshan, Tangshan, Hebei 063001, P.R. China
Published online on: July 23, 2014 https://doi.org/10.3892/mmr.2014.2416
Pages: 2099-2104

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Abstract

micro (mi)RNAs are short regulatory RNAs that negatively modulate protein expression at the post‑transcriptional level, and are being considered as novel therapeutic targets for the treatment of cancer. In the present study, an elevated expression level of circulating miR‑210 was observed in patients with esophageal squamous cell carcinoma (ESCC) for the first time, to the best of our knowledge, and the induction of miR‑210 under hypoxic conditions in ESCC was confirmed. Cell counting kit‑8 assay and bromodeoxyuridine incorporation assay indicated that miR‑210 markedly inhibited the proliferation of ESCC cells. In addition, the effect of miR‑210 on the cell cycle was examined. Transfection of miR‑210 resulted in a significant increase in the proportion of cells in G2/M phase. Polo‑like kinase 1 (PLK1) was investigated as a candidate target of miR‑210, which is a critical regulator of cell cycle transmission at multiple levels. It was demonstrated that miR‑210 reduced the levels of PLK1 protein by binding the 3' untranslated region of its mRNA. The results of the present study demonstrated that miR‑210 inhibited the proliferation of ESCC cells by inducing G2/M phase cell cycle arrest, and these effects of miR‑210 were mediated by the targeting of PLK1.

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