Alpha-fetoprotein activates AKT/mTOR signaling to promote CXCR4 expression and migration of hepatoma cells

CXCR4, stromal cell-derived factor-1α(SDF 1α) receptor, stimulates growth and metastasis of hepatocellular carcinoma (HCC). Alpha-fetoprotein(AFP) governs the expression of some metastasis-related genes. Here we report that AFP and CXCR4 levels correlated in HCC tissues. AFP-expressing vectors induc...

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Autores principales: Zhu, Mingyue, Guo, Junli, Xia, Hua, Li, Wei, Lu, Yan, Dong, Xu, Chen, Yi, Xie, Xieju, Fu, Shigan, Li, Mengsen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2015
Materias:
Research Paper
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4341465/
https://www.ncbi.nlm.nih.gov/pubmed/25815363
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author Zhu, Mingyue
Guo, Junli
Xia, Hua
Li, Wei
Lu, Yan
Dong, Xu
Chen, Yi
Xie, Xieju
Fu, Shigan
Li, Mengsen
author_facet Zhu, Mingyue
Guo, Junli
Xia, Hua
Li, Wei
Lu, Yan
Dong, Xu
Chen, Yi
Xie, Xieju
Fu, Shigan
Li, Mengsen
author_sort Zhu, Mingyue
collection PubMed
description CXCR4, stromal cell-derived factor-1α(SDF 1α) receptor, stimulates growth and metastasis of hepatocellular carcinoma (HCC). Alpha-fetoprotein(AFP) governs the expression of some metastasis-related genes. Here we report that AFP and CXCR4 levels correlated in HCC tissues. AFP-expressing vectors induced CXCR4. In agreement, AFP depletion by siRNA decreased CXCR4. AFP co-localized and interacted with PTEN, thus inducing CXCR4 by activating AKT(Ser473) phosphorylation. In turn, phospho-mTOR(Ser2448) entered the nucleus and bound the CXCR4 gene promoter. Thus, AFP promoted migration of HCC cells. In concusion, AFP induced CXCR4 by activating the AKT/mTOR signal pathway.
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spelling pubmed-43414652015-03-26 Alpha-fetoprotein activates AKT/mTOR signaling to promote CXCR4 expression and migration of hepatoma cells Zhu, Mingyue Guo, Junli Xia, Hua Li, Wei Lu, Yan Dong, Xu Chen, Yi Xie, Xieju Fu, Shigan Li, Mengsen Oncoscience Research Paper CXCR4, stromal cell-derived factor-1α(SDF 1α) receptor, stimulates growth and metastasis of hepatocellular carcinoma (HCC). Alpha-fetoprotein(AFP) governs the expression of some metastasis-related genes. Here we report that AFP and CXCR4 levels correlated in HCC tissues. AFP-expressing vectors induced CXCR4. In agreement, AFP depletion by siRNA decreased CXCR4. AFP co-localized and interacted with PTEN, thus inducing CXCR4 by activating AKT(Ser473) phosphorylation. In turn, phospho-mTOR(Ser2448) entered the nucleus and bound the CXCR4 gene promoter. Thus, AFP promoted migration of HCC cells. In concusion, AFP induced CXCR4 by activating the AKT/mTOR signal pathway. Impact Journals LLC 2015-01-06 /pmc/articles/PMC4341465/ /pubmed/25815363 Text en Copyright: © 2015 Zhu et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Zhu, Mingyue
Guo, Junli
Xia, Hua
Li, Wei
Lu, Yan
Dong, Xu
Chen, Yi
Xie, Xieju
Fu, Shigan
Li, Mengsen
Alpha-fetoprotein activates AKT/mTOR signaling to promote CXCR4 expression and migration of hepatoma cells
title Alpha-fetoprotein activates AKT/mTOR signaling to promote CXCR4 expression and migration of hepatoma cells
title_full Alpha-fetoprotein activates AKT/mTOR signaling to promote CXCR4 expression and migration of hepatoma cells
title_fullStr Alpha-fetoprotein activates AKT/mTOR signaling to promote CXCR4 expression and migration of hepatoma cells
title_full_unstemmed Alpha-fetoprotein activates AKT/mTOR signaling to promote CXCR4 expression and migration of hepatoma cells
title_short Alpha-fetoprotein activates AKT/mTOR signaling to promote CXCR4 expression and migration of hepatoma cells
title_sort alpha-fetoprotein activates akt/mtor signaling to promote cxcr4 expression and migration of hepatoma cells
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4341465/
https://www.ncbi.nlm.nih.gov/pubmed/25815363
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