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MED28 regulates the development of epithelial‐mesenchymal transition and invasion in human lung cancer cells (1097.14)
Author(s) -
Hsieh NienTsu,
Li ChunI,
Huang ChunYin,
Lee MingFen
Publication year - 2014
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.28.1_supplement.1097.14
Subject(s) - vimentin , epithelial–mesenchymal transition , gene knockdown , cancer research , matrigel , a549 cell , metastasis , mmp9 , biology , ectopic expression , extracellular matrix , gentamicin protection assay , cancer , lung cancer , microbiology and biotechnology , pathology , downregulation and upregulation , cell culture , medicine , immunohistochemistry , immunology , gene , angiogenesis , biochemistry , genetics
The development of the epithelial tumors from epithelial‐mesenchymal transition (EMT) to metastasis includes degradation and remodeling of the extracellular matrix and acquisition of a motile and invasive phenotype. MED28, facilitating transcriptional activation as a Mediator subunit, is also found highly expressed in epithelial tumors. Recently, we have reported that MED28 enhanced migration and invasion in human MCF7 and MDA‐MB‐231 breast cancer cells. The aim of this current study is to explore the role of MED28 in EMT and invasion in human non‐small cell lung cancer (NSCLC). Suppression of MED28 reduced the expression of vimentin, a mesenchymal marker, in human A549 NSCLC cells. In addition, TNFα induced EMT, whereas MED28 knockdown alleviated the morphological alterations. MED28 modulated TNFα‐induced Matrigel invasion and NFκB functional activity as assessed by heterologous promoter/reporter assay. The increased expression of several TNFα‐enhanced proteins, including MMP9, vimentin, p‐p65, and pIκB, was suppressed upon MED28 knockdown. Out data indicate a role of MED28 in the development of EMT and invasion in human NSCLC cells. Grant Funding Source : Supported by NSC101‐2320‐B‐309‐001 and NSC102‐2320‐B‐309‐001‐MY3 to M‐F Lee