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

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