4.2 Article

miR-942-5p Inhibits Proliferation, Metastasis, and Epithelial-Mesenchymal Transition in Colorectal Cancer by Targeting CCBE1

期刊

BIOMED RESEARCH INTERNATIONAL
卷 2021, 期 -, 页码 -

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HINDAWI LTD
DOI: 10.1155/2021/9951405

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资金

  1. National Natural Science Foundation of China [81772645, 81902385]
  2. Natural Science Foundation of the Jiangsu Higher Education Institutions of China [18KJB320025]
  3. Suzhou Institute of Biomedical Engineering and Technology of the Chinese Academy of Sciences [Y851401105]

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In CRC, downregulation of miR-942-5p inhibits proliferation and invasion of cancer cells, while upregulation of CCBE1 reverses these effects. CCBE1 is identified as a downstream target of miR-942-5p and is inversely correlated with its expression in CRC cells, suggesting that miR-942-5p may serve as a potential clinical biomarker for CRC diagnosis and therapy.
Although colorectal cancer (CRC) is common, there is a paucity of information regarding its molecular pathogenesis. Studies have shown that miRNAs play pivotal roles in the development and progression of CRC. There is a need to further investigate the biological functions of miRNAs in CRC. In particular, it has been reported that miR-942-5p exhibits tumor-suppressive properties. Thus, we analyzed the functional significance of miR-942-5p in CRC and the underlying molecular mechanisms. We found that miR-942-5p was downregulated in CRC tissues and cells. Cell Counting Kit-8, EdU, and colony formation assays revealed that the overexpression of miR-942-5p by mimics inhibited the proliferation of CRC cells. Use of the miR-942-5p inhibitor effectively enhanced the proliferative potential of CRC cells. Further, in vivo xenograft experiments confirmed these results. Increased expression of miR-942-5p suppressed the invasion, migration, and epithelial-mesenchymal transition of CRC cell lines, while decreased miR-942-5p expression had the opposite effect. CCBE1, a secretory molecule for lymphangiogenesis, was established as a downstream target of miR-942-5p, and its expression was inversely correlated with the expression of miR-942-5p in CRC cells. Additionally, cotransfection of the miR-942-5p inhibitor with si-CCBE1 into CRC cells reversed the effects induced by miR-942-5p overexpression. In conclusion, we confirmed that miR-942-5p exerts oncogenic actions in CRC by targeting CCBE1 and identified miR-942-5p as a potential clinical biomarker for CRC diagnosis and therapy.

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