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Loss of Med1/TRAP220 promotes the invasion and metastasis of human non-small-cell lung cancer cells by modulating the expression of metastasis-related genes.

Abstract
Med1/TRAP220 is an essential component of the TRAP/Mediator complex. In this study, we present a novel function of Med1 in human non-small-cell lung cancer (NSCLC) progression. We found that the loss of Med1 expression was strongly associated with increased rates of invasion and metastasis in NSCLC patients. Consistent with lung cancer patient data, the knockdown of Med1 in NSCLC cell lines led to an increase in cell migration and invasion. Med1-depleted cells displayed an increase in metastasis in a xenograft tumor model and in an in vivo metastasis assay. Moreover, a microarray analysis revealed that the mRNA levels of the metastasis-related genes uPAR, ID2, ID4, PTP4A1, PKP3, TGM2, PLD1, TIMP2, RGS2, and HOXA4 were altered upon Med1 knockdown. Collectively, these results suggest that the loss of Med1 increases the invasive potential of human NSCLC cells by modulating the expression of metastasis-related genes.
AuthorsHyun-Ju Kim, Mee Sook Roh, Choon Hee Son, Ae Jeong Kim, Hye Jin Jee, Naree Song, Minjee Kim, Su-Young Seo, Young Hyun Yoo, Jeanho Yun
JournalCancer letters (Cancer Lett) Vol. 321 Issue 2 Pg. 195-202 (Aug 28 2012) ISSN: 1872-7980 [Electronic] Ireland
PMID22342682 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2012 Elsevier Ireland Ltd. All rights reserved.
Chemical References
  • MED1 protein, human
  • Mediator Complex Subunit 1
  • RNA, Messenger
  • Transcription Factors
Topics
  • Animals
  • Blotting, Western
  • Carcinoma, Non-Small-Cell Lung (genetics, pathology)
  • Cell Line, Tumor
  • Gene Expression
  • Gene Expression Regulation
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Immunohistochemistry
  • Lung Neoplasms (genetics, metabolism, pathology)
  • Mediator Complex Subunit 1 (genetics, metabolism)
  • Mice
  • Neoplasm Invasiveness (genetics)
  • Neoplasm Metastasis (genetics)
  • RNA, Messenger (metabolism)
  • Real-Time Polymerase Chain Reaction
  • Transcription Factors (genetics, metabolism)

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