PTIP promotes recurrence and metastasis of hepatocellular carcinoma by regulating epithelial-mesenchymal transition
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Shusheng Leng1,*, Mingyang Yang2,*, Yanhua Zhao3,*, Jingfeng Zhao4, Zhijun Zeng5, Yunpeng Yang6, Jiatian Yuan1, Bo Lv1, Fan Jun1 and Bing Wang1
1General Surgery Department, Affiliated Hospital/Clinical Medical College of Chengdu University, Chengdu 610081, China
2Intensive Care Unit, The First People’s Hospital of Chengdu (Chengdu Combine Traditional Chinese and Western Medicine Hospital), Chengdu 610041, China
3Department of Laboratory Medicine/Clinical Research Center of Laboratory Medicine, West China Hospital of Sichuan University, Chengdu 610041, China
4General Surgery Department, Chongqing Dazu District People's Hospital, Chongqing 402360, China
5Department of Geratic Surgery, Xiangya Hospital, Central South University, Changsha 410008, China
6Department of Pathology, Affiliated Hospital/Clinical Medical College of Chengdu University, Chengdu 610081, China
*These authors have contributed equally to this work
Shusheng Leng, email: email@example.com
Jingfeng Zhao, email: firstname.lastname@example.org
Zhijun Zeng, email: Zengzhijun53@126.com
Keywords: PAX interacting protein1 (PTIP), hepatocelluar carcinoma, miRNA, epithelial-mesenchymal transition (EMT), metastasis
Received: October 11, 2016 Accepted: February 28, 2017 Published: March 22, 2017
Hepatocellular carcinoma (HCC) is one of the most lethal tumors worldwide, which is mainly due to the high recurrence and metastasis rate after hepatectomy. In this study, we found that PTIP expression was dramatically upregulated in human HCC tissues and cell lines. High expression of PTIP was shown to be associated with aggressive clinicopathological features, including liver cirrhosis, vascular invasion and advanced stage. In addition, PTIP overexpression was independently associated with shorter survival and increased HCC recurrence in patients. Knockdown of the PTIP expression significantly inhibited invasion and metastasis in vitro and in vivo, whereas ectopic expression of PTIP significantly promoted invasion and metastasis. Mechanistically, PTIP promotes HCC progress by facilitating epithelial-mesenchymal transition (EMT). Notably, we also found that PTIP might increase miR-374a expression to promote EMT and metastasis in HCC. In summary, our study identified PTIP as a new potential prognostic indicator and therapeutic target for HCC.
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