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

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• 作者：Hyun-Ju Kim^a ; ^b ; ¹ ; Mee Sook Roh^c ; ¹ ; Choon Hee Son^d ; Ae Jeong Kim^a ; ^b ; Hye Jin Jee^a ; ^b ; Naree Song^a ; ^b ; Minjee Kim^a ; ^b ; Su-Young Seo^e ; Young Hyun Yoo^b ; ^f ; Jeanho Yun^a ; ^b ; ^{yunj@dau.ac.kr}
• 关键词：Non-small-cell lung cancer ; Med1 ; Invasion ; Metastasis ; Transcription regulation
• 刊名：Cancer Letters
• 出版年：2012
• 期刊代码：44_03043835
• 类别：med
• 出版时间：28 August, 2012
• 卷：321
• 期：2
• 页码：195-202
• 文件大小：1107 K

摘要

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.