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Vitamin D attenuates MED28‐mediated cell growth and migration in human colon cancer cells
Author(s) -
Hsieh NienTsu,
Huang ChunYin,
Weng YuTing,
Lee MingFen
Publication year - 2016
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.30.1_supplement.917.13
Subject(s) - wnt signaling pathway , cancer research , cell growth , colorectal cancer , biology , cancer cell , cell migration , cancer , downregulation and upregulation , signal transduction , microbiology and biotechnology , cell , biochemistry , genetics , gene
Increasing lines of evidence indicate that vitamin D can prevent cancer progression by reducing cell proliferation and increasing cell differentiation. MED28 is both a Mediator subunit for transcriptional activation and an interactor with Grb2, Src kinases, actin cytoskeleton, and merlin. Our laboratory previously reported that MED28 regulates cell growth and migration in human breast cancer cells, indicating a role of MED28 in cancer development. Recently we have also found that MED28 mediates Wnt/β‐catenin signaling in human colon cancer cells. This study was to investigate the effect of vitamin D on MED28 in colorectal cancer. Our data indicated that MED28 not only upregulated Wnt/β‐catenin signaling but also increased the expression of fibronectin, a mesenchymal marker, and reduced the expression of E‐cadherin, an epithelial marker, in human colon cancer cells. Moreover, MED28 suppressed the expression of microRNA‐22 (miR‐22) which has been shown involved in suppressing tumor growth, migration, and invasion in colorectal cancer cells. However, vitamin D reversed these MED28‐mediated effects by downregulating the expression of MED28 at both mRNA and protein levels. Taken together, vitamin D suppresses cell growth and migration, at least partially, by targeting MED28‐regulated miR‐22 and Wnt/β‐catenin signaling in colorectal cancer. Support or Funding Information This work was supported by the grant NSC102‐2320‐B‐309‐001‐MY3 to M‐F Lee.