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Competing interests The authors declare that they have no competing interests. Authors’ contributions ZH, QC and XY conceived and designed the study, performed the experiments and wrote the paper. ZH and XY contributed to the writing and to the

critical reading of the paper. ZH, QC, LL performed patient collection and clinical data interpretation. ZH and LL participated performed the statistical analysis. All authors read and approved the final manuscript.”
“Introduction Nasopharyngeal carcinoma (NPC) is an epithelial malignant tumor with a high incidence in southern China and Southeast Asia. Radiotherapy is a dominant treatment approach for NPC. Primary tumor volume (GTV-P) is known to be positively correlated with the prognosis of NPC [1, 2]. Despite recently increased use of intensity-modulated radiation therapy (IMRT), GTV-P is still an independent selleck chemicals prognostic indicator for treatment outcome of NPC, and has correlations with T classification, cervical lymph node metastasis as well Lenvatinib purchase as post-treatment distant metastasis [3, 4]. Tumor volume is known to be positively correlated with the proliferation ability of tumor cells. Thus further understanding of molecular mechanisms underlying abnormal proliferation of NPC cells will help develop novel options for the diagnosis, therapy and prognosis of NPC. Metastasis-associated gene 1 (MTA1) has been implicated in the carcinogenesis and metastasis of

a variety of human cancers [5–7]. In particular, recent studies suggest the prognostic value of MTA1 in NPC because MTA1 overexpression was an independent prognostic factor for poor overall survival of NPC patients [8, 9]. Our recent study provided direct evidence that MTA1 regulated actin cytoskeleton reorganization to promote NPC metastasis [7]. However, the role of MTA1 in NPC cell proliferation is not clear. In the present study, we employed both gain and loss of function approaches to investigate the role of MTA1 in NPC growth. We examined the effects of MTA1 overexpression or knockdown on NPC cell proliferation, cell-cycle distribution, and colony formation in vitro. In addition, we evaluated the effects of MTA1 knockdown on NPC xenograft growth in nude mice.