Xiaoling Song1,2,3,4, Minghui Zhu5, Fahong Zhang6, Fei Zhang1,2,3,4, Yijian Zhang1,2,3,4, Yunping Hu1,2,3,4, Lin Jiang1,2,3,4, Yajuan Hao1,2,3,4, Shili Chen1,2,3,4, Qin Zhu1,2,3,4, Wen Huang1,2,3,4, Jianhua Lu1, Jun Gu1, Wei Gong1,2,3,4, Maolan Li1,2,3,4, Yingbin Liu1,2,3,4. 1. Department of General Surgery and Laboratory of General Surgery, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. 2. Shanghai Key Laboratory of Biliary Tract Disease Research, Shanghai, China. 3. Shanghai Research Center of Biliary Tract Disease, Shanghai, China. 4. Institute of Biliary Tract Disease, Shanghai Jiao Tong University School of Medicine, Shanghai, China. 5. Department of Hepatobiliary Surgery, The Third Affiliated Hospital to Wenzhou Medical University, Zhejiang, China. 6. Department of Gastroenterology, The First People's Hospital of Xiaoshan, Zhejiang, China.
Abstract
BACKGROUND/AIMS: The role of ZFX in tumourigenesis is unclear. We aimed to study ZFX expression, regulation, and function and the clinical implications of this protein in human pancreatic cancer (PCa). METHODS: One hundred and twenty patients with histologically confirmed PCa who underwent surgery were recruited for this study. Tumour samples and PCa cell lines were used to examine ZFX. Various cell functions related to tumourigenesis were assessed. In vivo mouse tumour xenografts were used to confirm the in vitro results. RESULTS: Patients with ZFX-positive tumours had worse overall survival than patients with ZFX-negative tumours. The depletion of ZFX using lentiviral shRNAs significantly inhibited cell proliferation by inducing cell cycle arrest in G0/G1 phase and resulted in increased cell apoptosis and invasive repression. In vivo studies confirmed that ZFX promoted tumour growth. Mechanistically, MAPK pathway activation was involved in the oncogenic functions of ZFX. CONCLUSIONS: ZFX acts as a putative oncogene in PCa and could be a novel therapeutic target for this disease.
BACKGROUND/AIMS: The role of ZFX in tumourigenesis is unclear. We aimed to study ZFX expression, regulation, and function and the clinical implications of this protein in humanpancreatic cancer (PCa). METHODS: One hundred and twenty patients with histologically confirmed PCa who underwent surgery were recruited for this study. Tumour samples and PCa cell lines were used to examine ZFX. Various cell functions related to tumourigenesis were assessed. In vivo mousetumour xenografts were used to confirm the in vitro results. RESULTS:Patients with ZFX-positive tumours had worse overall survival than patients with ZFX-negative tumours. The depletion of ZFX using lentiviral shRNAs significantly inhibited cell proliferation by inducing cell cycle arrest in G0/G1 phase and resulted in increased cell apoptosis and invasive repression. In vivo studies confirmed that ZFX promoted tumour growth. Mechanistically, MAPK pathway activation was involved in the oncogenic functions of ZFX. CONCLUSIONS:ZFX acts as a putative oncogene in PCa and could be a novel therapeutic target for this disease.