Zinc Finger Protein 217 (ZNF217)

ZNF217 can attenuate apoptotic signals resulting from telomere dysfunction as well as from doxorubicin-induced DNA damage, and that silencing ZNF217 with siRNA restored sensitivity to doxorubicin. Elevated ZNF217 led to increased phosphorylation of Akt1, whereas inhibition of the phosphatidylinositol-3 kinase pathway and Akt phosphorylation decreased ZNF217 protein levels and increased sensitivity to doxorubicin. ZNF217 may promote neoplastic transformation by increasing cell survival during telomeric crisis, and may promote later stages of malignancy by increasing cell survival during chemotherapy.ZNF217 was found to be centrally located in the 260-kb common region of amplification, transcribed in multiple normal tissues, and overexpressed in all cell lines and tumors in which it was amplified.