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ZNF692 promotes proliferation and cell mobility in lung adenocarcinoma
Quanli Zhang1, Xiufen Zheng1, Qi Sun2
1Department of Clinical Pharmacy, China Pharmaceutical University, Nanjing, 210009, PR China; Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Nanjing, 210009, PR China; Department of Thoracic Surgery, Jiangsu Cancer Hospital, Institute Affiliated to Nanjing Medical University, Cancer Institute of Jiangsu Province, Baiziting 42, Xuanwu District, Nanjing, 210009, PR China.
Abstract:
By analyzing The Cancer Genome Atlas (TCGA) datasets, we discovered that the zinc finger protein 692 (ZNF692) were over-expressed in Lung adenocarcinoma (LUAD) tissues compared to adjacent non-tumor tissues (P < 0.0001). In this study, we investigated the function of ZNF692 in the progression of LUAD. We found that ZNF692 knockdown inhibited LUAD cells proliferation, migration, and invasion both in vitro and in vivo. And LUAD cell apoptosis was induced following the down-regulation of ZNF692. Our results show that ZNF692 is over-expressed in LUAD tissues compared to adjacent normal tissues, and hyper-expression of ZNF692 in LUAD is an independent risk factor for worse overall survival in LUAD patients (HR: 8.800, 95%CI: 1.082-71.560, P = 0.042) by Tissue Microarray stain assay (TMA). GO analysis indicated that most genes were enriched in metabolic process which were associated highly with ZNF692 levels. Collectively, our results suggested that ZNF692 may serve as a potential oncogene and biomarker in LUAD by influencing cell metabolism.
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