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Effect of MED28 on epithelial‐mesenchymal transition in human colorectal cancer cells
Author(s) -
Li Po-Chen,
Hsieh Nien-Tsu,
Chang Yu-Tsen,
Lee Ming-Fen
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.05066
Subject(s) - epithelial–mesenchymal transition , wnt signaling pathway , vimentin , mesenchymal stem cell , cancer research , mediator , colorectal cancer , biology , microbiology and biotechnology , gene knockdown , signal transduction , cancer , metastasis , cell culture , immunology , genetics , immunohistochemistry
Mammalian Mediator complex plays an important role in transcriptional activation by bridging RNA polymerase II and transcriptional machinery. Multiple Mediator subunits have been implicated in human diseases including cancer development. Our laboratory has previously reported that MED28, a Mediator subunit, mediates Wnt/β‐catenin signaling and promotes cell growth in human colorectal cancer (CRC) cells. The objective of the current study is to investigate the effect of MED28 on epithelial‐mesenchymal transition in CRC in addition to cell growth. Suppression of MED28 attenuated the expression of several mesenchymal biomarkers including vimentin and transcription factors Snail and Slug, but increased the expression of E‐cadherin, an epithelial biomarker; however, overexpression of MED28 reversed the reciprocal change of epithelial and mesenchymal biomarkers. The underlying molecular mechanism is currently under investigation. Our data indicate that MED28 modulates the development of epithelial‐mesenchymal transition in human CRC cells, further reinforcing the significance of MED28 in the progression of malignancy in CRC. Support or Funding Information This work was supported by the grant MOST 106‐2320‐B‐039‐062‐MY3 to M‐F Lee.