FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1817869836> ?p ?o ?g. }

• W1817869836 endingPage "12208" @default.
• W1817869836 startingPage "12196" @default.
• W1817869836 abstract "// Mingyue Zhu 1, 2, * , Junli Guo 1, 3, * , Wei Li 1, 2 , Yan Lu 1, 2 , Shigan Fu 1 , Xieju Xie 4 , Hua Xia 1, 2 , Xu Dong 1, 2 , Yi Chen 1, 2 , Ming Quan 3 , Shaojiang Zheng 1, 5 , Keping Xie 3 , Mengsen Li 1, 2 1 Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical College, Haikou, Hainan 571199, P. R. China 2 Key Laboratory of Molecular Biology, Hainan Medical College, Haikou, Hainan 571199, P. R. China 3 Department of Gastroenterology, Hepatology & Nutrition, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA 4 Department of Physiology and Pathophysiology, Hainan Medical College, Haikou, Hainan 571199, P. R. China 5 Tumor Institute, Affiliated Hospital of Hainan Medical College, Haikou, Hainan 570102, P. R. China * These authors have contributed equally to this work Correspondence to: Mengsen Li, e-mail: mengsenli@163.com Keping Xie, e-mail: kepxie@mdanderson.org Keywords: AFP, HBx, PI3K/mTOR signaling, Liver cells, Hepatocarcinogenesis Received: October 10, 2014      Accepted: December 11, 2014      Published: January 21, 2015 ABSTRACT The hepatitis B virus (HBV)-X protein (HBx) induces malignant transformation of liver cells, and elevated expression of alpha-fetoprotein (AFP) is a significant biomarker of hepatocarcinogenesis. However, the role of AFP in HBV-related hepatocarcinogenesis is unclear. In this study, we investigated the regulatory impact of AFP expression on HBx-mediated malignant transformation of human hepatocytes. We found that HBV induced the expression of AFP before that of oncogenes, e.g ., Src, Ras and chemokine (C-X-C motif) receptor 4 (CXCR4), and AFP activated protein kinase B (AKT) and mammalian target of rapamycin (mTOR) in HBV-related HCC tissues and in human liver cells transfected with HBx. Cytoplasmic AFP interacted with and inhibited phosphatase and tensin homolog deleted on chromosome 10 (PTEN), activating the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway and promoting mTOR-mediated stimulation of the transcription factor hypoxia inducible factor-1α (HIF-1α), and therefore led to the activation of the promoters of Src, CXCR4, and Ras genes. On the contrary, reduced expression of AFP by siRNA resulted in the repression of p-mTOR, pAKT, Src, CXCR4, and Ras in human malignant liver cells. Taken together, for the first time our study indicates that HBx-induced AFP expression critically promote malignant transformation in liver cells through the activation of PI3K/mTOR signaling." @default.
• W1817869836 created "2016-06-24" @default.
• W1817869836 creator A5000432967 @default.
• W1817869836 creator A5001282129 @default.
• W1817869836 creator A5005741943 @default.
• W1817869836 creator A5006940824 @default.
• W1817869836 creator A5021641984 @default.
• W1817869836 creator A5023442400 @default.
• W1817869836 creator A5030936950 @default.
• W1817869836 creator A5045897433 @default.
• W1817869836 creator A5049393970 @default.
• W1817869836 creator A5053149750 @default.
• W1817869836 creator A5059889471 @default.
• W1817869836 creator A5063488503 @default.
• W1817869836 creator A5063800558 @default.
• W1817869836 date "2015-01-21" @default.
• W1817869836 modified "2023-10-16" @default.
• W1817869836 title "Hepatitis B virus X protein induces expression of alpha-fetoprotein and activates PI3K/mTOR signaling pathway in liver cells" @default.
• W1817869836 cites W1480852720 @default.
• W1817869836 cites W1546930353 @default.
• W1817869836 cites W1841699403 @default.
• W1817869836 cites W1967637189 @default.
• W1817869836 cites W1969248336 @default.
• W1817869836 cites W1969360083 @default.
• W1817869836 cites W1974522159 @default.
• W1817869836 cites W1978110996 @default.
• W1817869836 cites W1983420558 @default.
• W1817869836 cites W1983796564 @default.
• W1817869836 cites W1984131437 @default.
• W1817869836 cites W1987592728 @default.
• W1817869836 cites W1989312510 @default.
• W1817869836 cites W1990196941 @default.
• W1817869836 cites W1996865638 @default.
• W1817869836 cites W1998039589 @default.
• W1817869836 cites W2003459252 @default.
• W1817869836 cites W2007090162 @default.
• W1817869836 cites W2007333527 @default.
• W1817869836 cites W2009641609 @default.
• W1817869836 cites W2012409389 @default.
• W1817869836 cites W2015954989 @default.
• W1817869836 cites W2016358101 @default.
• W1817869836 cites W2016876202 @default.
• W1817869836 cites W2025893687 @default.
• W1817869836 cites W2039576757 @default.
• W1817869836 cites W2058349670 @default.
• W1817869836 cites W2065915723 @default.
• W1817869836 cites W2066425902 @default.
• W1817869836 cites W2068127752 @default.
• W1817869836 cites W2077623588 @default.
• W1817869836 cites W2079899695 @default.
• W1817869836 cites W2089336126 @default.
• W1817869836 cites W2090817847 @default.
• W1817869836 cites W2094573329 @default.
• W1817869836 cites W2106787323 @default.
• W1817869836 cites W2115413477 @default.
• W1817869836 cites W2116159404 @default.
• W1817869836 cites W2116600524 @default.
• W1817869836 cites W2123125812 @default.
• W1817869836 cites W2134123146 @default.
• W1817869836 cites W2134456945 @default.
• W1817869836 cites W2134748677 @default.
• W1817869836 cites W2135394461 @default.
• W1817869836 cites W2144715892 @default.
• W1817869836 cites W2147286234 @default.
• W1817869836 cites W2153209854 @default.
• W1817869836 cites W2164895949 @default.
• W1817869836 cites W2165941161 @default.
• W1817869836 cites W2537555591 @default.
• W1817869836 doi "https://doi.org/10.18632/oncotarget.2906" @default.
• W1817869836 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4494932" @default.
• W1817869836 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25682869" @default.
• W1817869836 hasPublicationYear "2015" @default.
• W1817869836 type Work @default.
• W1817869836 sameAs 1817869836 @default.
• W1817869836 citedByCount "57" @default.
• W1817869836 countsByYear W18178698362015 @default.
• W1817869836 countsByYear W18178698362016 @default.
• W1817869836 countsByYear W18178698362017 @default.
• W1817869836 countsByYear W18178698362018 @default.
• W1817869836 countsByYear W18178698362019 @default.
• W1817869836 countsByYear W18178698362020 @default.
• W1817869836 countsByYear W18178698362021 @default.
• W1817869836 countsByYear W18178698362022 @default.
• W1817869836 countsByYear W18178698362023 @default.
• W1817869836 crossrefType "journal-article" @default.
• W1817869836 hasAuthorship W1817869836A5000432967 @default.
• W1817869836 hasAuthorship W1817869836A5001282129 @default.
• W1817869836 hasAuthorship W1817869836A5005741943 @default.
• W1817869836 hasAuthorship W1817869836A5006940824 @default.
• W1817869836 hasAuthorship W1817869836A5021641984 @default.
• W1817869836 hasAuthorship W1817869836A5023442400 @default.
• W1817869836 hasAuthorship W1817869836A5030936950 @default.
• W1817869836 hasAuthorship W1817869836A5045897433 @default.
• W1817869836 hasAuthorship W1817869836A5049393970 @default.
• W1817869836 hasAuthorship W1817869836A5053149750 @default.
• W1817869836 hasAuthorship W1817869836A5059889471 @default.
• W1817869836 hasAuthorship W1817869836A5063488503 @default.
• W1817869836 hasAuthorship W1817869836A5063800558 @default.

• next