Overexpression of CXCR7 induces angiogenic capacity of human hepatocellular carcinoma cells via the AKT signaling pathway

Angiogenesis is essential for tumor growth, especially in hepatocellular carcinoma (HCC). The hypervascularity is associated with poor prognosis and highly invasive HCC. The C-X-C chemokine receptor type 7 (CXCR7) has been implied overexpressed in many tumor types. Our study aimed to investigate the...

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Veröffentlicht in:Oncology reports 2016-10, Vol.36 (4), p.2275-2281
Hauptverfasser: Chen, Yuhui, Teng, Fei, Wang, Geying, Nie, Zhiyu
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container_title Oncology reports
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creator Chen, Yuhui
Teng, Fei
Wang, Geying
Nie, Zhiyu
description Angiogenesis is essential for tumor growth, especially in hepatocellular carcinoma (HCC). The hypervascularity is associated with poor prognosis and highly invasive HCC. The C-X-C chemokine receptor type 7 (CXCR7) has been implied overexpressed in many tumor types. Our study aimed to investigate the CXCR7 function in HCC. The tube formation, Transwell migration assay of human umbilical vein endothelial cells (HUVECs) and chicken chorioallantoic membrane (CAM) assay were used. We confirmed that CXCR7 induces angiogenic capacity. Moreover, overexpressing CXCR7 increased the phosphorylated (but not total) AKT expression in HCC cells. Furthermore, overexpressing CXCR7 increased the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-8 in HCC cells. Additionally, inhibition of AKT by LY294002 abrogated CXCR7-induced angiogenic capacity in HCC cells. Our study suggested that CXCR7 plays an important pro-angiogenic role in HCC via activation of the AKT pathway. So CXCR7 may be a potential target for anti-angiogenic therapy in HCC.
doi_str_mv 10.3892/or.2016.5045
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migration</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell receptors</topic><topic>Development and progression</topic><topic>Embryos</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Hepatitis</topic><topic>hepatocellular carcinoma</topic><topic>Hepatoma</topic><topic>Human Umbilical Vein Endothelial Cells</topic><topic>Humans</topic><topic>Interleukin-6 - biosynthesis</topic><topic>Interleukin-6 - genetics</topic><topic>Interleukin-8 - biosynthesis</topic><topic>Interleukin-8 - genetics</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - pathology</topic><topic>Metastasis</topic><topic>Molecular Targeted Therapy</topic><topic>Neovascularization</topic><topic>Neovascularization, Pathologic - drug therapy</topic><topic>Neovascularization, Pathologic - genetics</topic><topic>Neovascularization, Pathologic - pathology</topic><topic>Physiology</topic><topic>Proto-Oncogene Proteins c-akt - biosynthesis</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Receptors, CXCR - biosynthesis</topic><topic>Receptors, CXCR - genetics</topic><topic>Signal Transduction - genetics</topic><topic>Tumors</topic><topic>Vascular endothelial growth factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Yuhui</creatorcontrib><creatorcontrib>Teng, Fei</creatorcontrib><creatorcontrib>Wang, Geying</creatorcontrib><creatorcontrib>Nie, Zhiyu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health &amp; 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The hypervascularity is associated with poor prognosis and highly invasive HCC. The C-X-C chemokine receptor type 7 (CXCR7) has been implied overexpressed in many tumor types. Our study aimed to investigate the CXCR7 function in HCC. The tube formation, Transwell migration assay of human umbilical vein endothelial cells (HUVECs) and chicken chorioallantoic membrane (CAM) assay were used. We confirmed that CXCR7 induces angiogenic capacity. Moreover, overexpressing CXCR7 increased the phosphorylated (but not total) AKT expression in HCC cells. Furthermore, overexpressing CXCR7 increased the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-8 in HCC cells. Additionally, inhibition of AKT by LY294002 abrogated CXCR7-induced angiogenic capacity in HCC cells. Our study suggested that CXCR7 plays an important pro-angiogenic role in HCC via activation of the AKT pathway. 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source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
subjects Angiogenesis
C-X-C chemokine receptor type 7
Carcinoma, Hepatocellular - drug therapy
Carcinoma, Hepatocellular - genetics
Carcinoma, Hepatocellular - pathology
Care and treatment
Cell adhesion & migration
Cell growth
Cell Line, Tumor
Cell receptors
Development and progression
Embryos
Gene expression
Gene Expression Regulation, Neoplastic
Genetic aspects
Health aspects
Hepatitis
hepatocellular carcinoma
Hepatoma
Human Umbilical Vein Endothelial Cells
Humans
Interleukin-6 - biosynthesis
Interleukin-6 - genetics
Interleukin-8 - biosynthesis
Interleukin-8 - genetics
Liver cancer
Liver Neoplasms - genetics
Liver Neoplasms - pathology
Metastasis
Molecular Targeted Therapy
Neovascularization
Neovascularization, Pathologic - drug therapy
Neovascularization, Pathologic - genetics
Neovascularization, Pathologic - pathology
Physiology
Proto-Oncogene Proteins c-akt - biosynthesis
Proto-Oncogene Proteins c-akt - genetics
Receptors, CXCR - biosynthesis
Receptors, CXCR - genetics
Signal Transduction - genetics
Tumors
Vascular endothelial growth factor
title Overexpression of CXCR7 induces angiogenic capacity of human hepatocellular carcinoma cells via the AKT signaling pathway
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