Fucosyltransferase 8 regulation and breast cancer suppression by transcription factor activator protein 2γ

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  • Minxing Ma
    Department of Oncology The Fifth People's Hospital of Qinghai Province Xining China
  • Dong Guo
    Department of Central Lab Cheeloo College of Medicine Weihai Municipal Hospital Shandong University Weihai China
  • Zengqi Tan
    Key Laboratory of Resource Biology and Biotechnology in Western China Ministry of Education Joint International Research Laboratory of Glycobiology and Medicinal Chemistry College of Life Sciences Northwest University Xi'an China
  • Jun Du
    Department of Oncology The Fifth People's Hospital of Qinghai Province Xining China
  • Feng Guan
    Key Laboratory of Resource Biology and Biotechnology in Western China Ministry of Education Joint International Research Laboratory of Glycobiology and Medicinal Chemistry College of Life Sciences Northwest University Xi'an China
  • Xiang Li
    Institute of Hematology School of Medicine Northwest University Xi'an China

書誌事項

公開日
2021-06-12
権利情報
  • http://creativecommons.org/licenses/by-nc/4.0/
DOI
  • 10.1111/cas.14987
公開者
Wiley

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<jats:title>Abstract</jats:title><jats:p>Alterations of glycosyltransferase expression are often associated with tumor occurrence and progression. Among the many glycosyltransferases, increased expression of fucosyltransferase 8 (FUT8) has been frequently observed to be involved in progression and metastasis of various types of cancer. The regulatory mechanisms of FUT8 expression remain unclear. FUT8 expression was shown, in this study, to be elevated in breast cancer. Systematic analysis revealed that transcription factor activator protein 2γ (AP‐2γ) is the target gene of microRNA‐10b (miR‐10b), which we previously identified as a positive regulator of FUT8. Overexpression of AP‐2γ inhibited FUT8 expression, with associated reduction of cell invasiveness and migration ability. AP‐2γ was capable of binding to transcription factor STAT3, and phosphorylation of STAT3 induced transcription of the FUT8 gene. On the basis of our findings, we propose that binding of AP‐2γ to STAT3 results in formation of the AP‐2γ/STAT3 complex and consequent inhibition of STAT3 phosphorylation, thereby preventing entry of p‐STAT3 into the nucleus to initiate FUT8 transcription. This study clarifies the molecular mechanisms whereby transcription factor AP‐2γ regulates FUT8 expression in breast cancer.</jats:p>

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