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Background  Epigenetic abnormalities play important roles in nasopharyngeal cancer (NPC), however, the epigenetic changes associated with abnormal cell proliferation remain unclear.    Methods  We detected epigenetic change of  ZNF671  in NPC tissues and cell lines by bisulfite pyrosequencing. We evaluated zinc finger protein 671 ( ZNF671 ) expression in NPC cell lines and clinical tissues using real-time PCR and western blotting. Then, we established NPC cell lines that stably overexpressed  ZNF671  and knocked down  ZNF671  expression to explore its function in NPC in vitro and in vivo. Additionally, we investigated the potential mechanism of  ZNF671  by identifying the mitotic spindle and G2/M checkpoint pathways pathway downstream genes using gene set enrichment analysis, flow cytometry and western blotting.    Results    ZNF671  was hypermethylated in NPC tissues and cell lines. The mRNA and protein expression of  ZNF671  was down-regulated in NPC tissues and cell lines and the mRNA expression could be upregulated after the demethylation agent 5-aza-2′-deoxycytidine treatment. Overexpression of  ZNF671  suppressed NPC cell proliferation and colony formation in vitro; silencing  ZNF671  using a siRNA had the opposite effects. Additionally, overexpression of  ZNF671  reduced the tumorigenicity of NPC cells in xenograft model in vivo. The mechanism study determined that overexpressing  ZNF671  induced S phase arrest in NPC cells by upregulating p21 and downregulating cyclin D1 and c-myc.    Conclusions  Epigenetic mediated zinc finger protein 671 downregulation promotes cell proliferation and enhances tumorigenicity by inhibiting cell cycle arrest in NPC, which may represent a novel potential therapeutic target.    Electronic supplementary material  The online version of this article (10.1186/s13046-017-0621-2) contains supplementary material, which is available to authorized users.

journal of experimental and clinical cancer research

Epigenetic mediated zinc finger protein 671 downregulation promotes cell proliferation and tumorigenicity in nasopharyngeal carcinoma by inhibiting cell cycle arrest