4.8 Article Retracted Publication

被撤回的出版物: YAP1-induced MALAT1 promotes epithelial-mesenchymal transition and angiogenesis by sponging miR-126-5p in colorectal cancer (Retracted article. See JUL, 2023)

Journal

ONCOGENE
Volume 38, Issue 14, Pages 2627-2644

Publisher

SPRINGERNATURE
DOI: 10.1038/s41388-018-0628-y

Keywords

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Funding

  1. National Natural Science Foundation of China [81560385]
  2. Natural Science Foundation of Xinjiang Uygur Autonomous Region [2015211C136]
  3. Medical Scientific and Technological Research Project of Henan Province [201702027]
  4. China Postdoctoral Science Foundation [2017M610462]
  5. Youth Innovation Fund Project of The First Affiliated Hospital of Zhengzhou University [YNQN2017035]

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Yes-associated protein 1 (YAP1) exerts significant effects in various malignancies. However, the oncogenic role of YAP1 remains controversial, and the mechanism by which YAP1 regulates non-coding RNAs is still largely unknown. The present study aimed to assess the effect of YAP1 on the malignant behaviors of colorectal carcinoma (CRC) and explore the underlying regulatory mechanism of the YAP1-MALAT1-miR-126-5p axis. YAP1 was highly expressed in CRC tissues as assessed by GSE20916 and its expression was negatively correlated with overall survival in 83 CRC cases. Meanwhile, YAP1 promoted proliferation, invasion, and migration in colon cancer cells, in vitro and in vivo. MALAT1 was obviously expressed, with differential expression of 11 lncRNAs in HCT116 cells after transfection with siYAP1 or si-Ctl. Based on bioinformatics prediction, immunoprecipitation (IP), and chromatin immunoprecipitation (ChIP), the interaction of YAP1 with TCF4/beta-catenin was regulated by MALAT1. Bioinformatics prediction, dual luciferase assay, RNA-IP, and RNA pulldown assay demonstrated that YAP1-induced MALAT1 promoted the expression of metastasis-associated molecules such as VEGFA, SLUG, and TWIST, by sponging miR-126-5p in CRC. These findings indicated that the YAP1-MALAT1-miR126-5p axis could control angiogenesis and epithelial-mesenchymal transition in CRC, providing potential biomarkers and therapeutic targets for CRC.

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