Abstract. Metastasis-associated gene 1 (MTA1) is involved in the carcinogenesis and metastasis of many human carcinomas. However, its exact role in non-small cell lung cancer (NSCLC) is still unclear. Using immunohistochemistry analysis, we recently identified MTA1 to be associated with the progression of NSCLC. Here, we carried out further analysis on the effect of MTA1 knockdown in an NSCLC cell line on cell functions and the global microRNA (miRNA) expression profile. We succeeded in establishing the MTA1 knockdown NSCLC cell line using RNA interference (RNAi), and found that the silencing of MTA1 resulted in the effective inhibition of the invasive ability of NSCLC cells, but not of the cell growth in vitro. We performed an miRNA microarray analysis and demonstrated for the first time that MTA1 knockdown significantly changed the expression of some miRNAs in NSCLC cells. Among them, some have a well-characterized association with cancer progression, e.g. miR-125b, miR-210, miR-103, miR-194 and miR-500. In summary, it is evident from our results that MTA1 functions in regulating the invasive phenotype of lung cancer cells and this regulation may be through altered miRNA expression. The interaction between MTA1 and the miRNAs which contributes to lung cancer is worthy of further investigation.
BackgroundThe prognostic value of metastasis-associated gene 1 (MTA1) in nasopharyngeal carcinoma (NPC) has been suggested. However, there is still no direct evidence that MTA1 promotes NPC growth in vivo. In this study, we aimed to investigate the function of MTA1 in the regulation of NPC cell proliferation and tumorigenesis in vitro and in vivo.MethodsStable MTA1 knockdown or overexpression NPC cell lines were employed. The effects of MTA1 depletion or overexpression on cell proliferation, colony formation, cell cycle progression were examined by MTT, colony formation and flow cytometry assay. The effects of MTA1 depletion on tumor growth in vivo were examined in mouse xenograft model.ResultsMTA1 knockdown or overexpression drastically changed the proliferation, colony formation and cell cycle of NPC cells in vitro. MTA1 depletion significantly suppressed NPC tumorigenesis in vivo.ConclusionMTA1 promotes NPC cell proliferation via enhancing G1 to S phase transition, leading to increased tumor growth. Targeting MTA1 is a promising approach to reduce tumor burden of NPC.
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