Loss of Pten synergizes with c-Met to promote hepatocellular carcinoma development via mTORC2 pathway
失Pten与c- Met协同通过mTORC2通路促进肝细胞癌的发生发展
作者: Zhong XuJunjie HuHui CaoMaria G PiloAntonio CiglianoZixuan ShaoMeng XuSilvia RibbackFrank DombrowskiDiego F CalvisiXin Chen
作者单位: 1Department of Gastroenterology, Guizhou Provincial People’s Hospital, The Affiliated People’s Hospital of Guizhou Medical University, Guiyang, PR China
2Department of Bioengineering and Therapeutic Sciences and Liver Center, University of California, San Francisco, CA, USA
3School of Pharmacy, Hubei University of Chinese Medicine, Wuhan, PR China
4Department of Oncology, Guizhou Provincial People’s Hospital, Guiyang, PR China
5Institute of Pathology, University of Greifswald, Greifswald, Germany
6Lowell High School, San Francisco, CA, USA
7Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi’an, PR China
刊名: Experimental & Molecular Medicine, 2018, Vol.50 (1), pp.e417-e417
来源数据库: Springer Nature Journal
DOI: 10.1038/emm.2017.158
英文摘要: Abstract(#br)Hepatocellular carcinoma (HCC) is a deadly malignancy with limited treatment options. Activation of the AKT/mTOR cascade is one of the most frequent events along hepatocarcinogenesis. mTOR is a serine/threonine kinase and presents in two distinct complexes: mTORC1 and mTORC2. While mTORC1 has been extensively studied in HCC, the functional contribution of mTORC2 during hepatocarcinogenesis has not been well characterized, especially in vivo . Pten expression is one of the major mechanisms leading to the aberrant activation of the AKT/mTOR signaling. Here, we show that concomitant downregulation of Pten and upregulation of c-Met occurs in a subset of human HCC, mainly characterized by poor prognosis. Using CRISPR-based gene editing in combination with hydrodynamic injection,...
全文获取路径: Springer Nature  (合作)
影响因子:2.573 (2012)