ZNF259 inhibits non-small cell lung cancer cells proliferation and invasion by FAK-AKT signaling

• DOI: 10.2147/cmar.s150614
• Publication Date: 2017-12-14T01:33:09Z
• Authors: Yuemei Shan; Wei Cao; Tao Wang; Guiyang Jiang; Yong Zhang; Xianghong Yang
• Keywords: 0303 health sciences; proliferation; Neoplasms. Tumors. Oncology. Including cancer and carcinogens; NSCLC; invasion; 3. Good health; 03 medical and health sciences; Cancer Management and Research; FAK signaling; ZNF259; AKT signaling; RC254-282; Original Research

Zinc finger protein 259 (ZNF259) is known to play essential roles in embryonic development and cell cycle regulation. However, its expression pattern clinicopathological relevance remain unclear.A total of 114 lung cancer specimens were collected. The ZNF259 was measured between the tissues adjacent normal by immunohistochemical staining Western blotting. Moreover, correlation with features analyzed cases cancer. Additionally, depleted cells order analyze effect cancer.Immunohistochemical revealed significantly lower than (53.5% vs 71.4%, P<0.001). In addition, downregulation associated larger tumor size (P=0.001), advanced TNM stage (P=0.002), positive lymph node metastasis (P=0.02). blotting 20 paired samples levels those corresponding (P=0.0032). Depletion resulted enhanced p-FAK p-AKT, CyclinD1, MMP2, which turn increased proliferation invasion cells. effects depletion reversed treatment specific FAK or AKT inhibitors.ZNF259 correlated non-small (NSCLC) serves as a predictor adverse clinical outcome NSCLC patients. inhibitory on can be attributed CyclinD1 MMP2 via inactivation FAK-AKT pathway.