CXCL12-induced upregulation of FOXM1 expression promotes human glioblastoma cell invasion

•CXCL12 regulates FOXM1.•AKT pathway regulates FOXM1.•CXCL12 enhances cell invasion. Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor; it is highly aggressive and is associated with a poor prognosis. Binding of the chemokine CXCL12 to its receptors (CXCR4 and CXCR7) con...

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Veröffentlicht in:Biochemical and biophysical research communications 2014-04, Vol.447 (1), p.1-6
Hauptverfasser: Wang, Shengwen, Zhang, Shanyi, Li, Junliang, Xu, Xinke, Weng, Yinlun, Zheng, Meiguang, Ouyang, Leping, Li, Fangcheng
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container_issue 1
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container_title Biochemical and biophysical research communications
container_volume 447
creator Wang, Shengwen
Zhang, Shanyi
Li, Junliang
Xu, Xinke
Weng, Yinlun
Zheng, Meiguang
Ouyang, Leping
Li, Fangcheng
description •CXCL12 regulates FOXM1.•AKT pathway regulates FOXM1.•CXCL12 enhances cell invasion. Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor; it is highly aggressive and is associated with a poor prognosis. Binding of the chemokine CXCL12 to its receptors (CXCR4 and CXCR7) contributes to the activation of many downstream signaling pathways and promotes the invasion of various malignant tumor cells, including GBM cells. FOXM1, a transcription factor involved in cell cycle regulation, is overexpressed in GBM and is involved in GBM progression. However, the molecular mechanisms by which CXCL12 promotes the invasion of human GBM cells remain unclear. In this study, we demonstrate that CXCL12 increases the production of FOXM1 by binding to CXCR4 in GBM cell lines. Furthermore, pretreatment with an inhibitor of the PI3K/AKT pathway abrogated the CXCL12-induced expression of FOXM1. In addition, there was a positive correlation between CXCL12/CXCR4 expression and FOXM1 expression in human malignant glioma tissues. Finally, a functional assay revealed that CXCL12 does not stimulate GBM cell invasion when FOXM1 expression is silenced using a small interfering RNA (siRNA). Collectively, these findings suggest that CXCL12 promotes GBM cell invasion in part by increasing the expression of FOXM1, which is mediated in part by a PI3K/AKT-dependent mechanism in vitro.
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Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor; it is highly aggressive and is associated with a poor prognosis. Binding of the chemokine CXCL12 to its receptors (CXCR4 and CXCR7) contributes to the activation of many downstream signaling pathways and promotes the invasion of various malignant tumor cells, including GBM cells. FOXM1, a transcription factor involved in cell cycle regulation, is overexpressed in GBM and is involved in GBM progression. However, the molecular mechanisms by which CXCL12 promotes the invasion of human GBM cells remain unclear. In this study, we demonstrate that CXCL12 increases the production of FOXM1 by binding to CXCR4 in GBM cell lines. Furthermore, pretreatment with an inhibitor of the PI3K/AKT pathway abrogated the CXCL12-induced expression of FOXM1. In addition, there was a positive correlation between CXCL12/CXCR4 expression and FOXM1 expression in human malignant glioma tissues. Finally, a functional assay revealed that CXCL12 does not stimulate GBM cell invasion when FOXM1 expression is silenced using a small interfering RNA (siRNA). Collectively, these findings suggest that CXCL12 promotes GBM cell invasion in part by increasing the expression of FOXM1, which is mediated in part by a PI3K/AKT-dependent mechanism in vitro.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2013.12.079</identifier><identifier>PMID: 24561124</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Astrocytoma - pathology ; Brain Neoplasms - metabolism ; Brain Neoplasms - pathology ; Cell Line, Tumor ; Chemokine ; Chemokine CXCL12 - biosynthesis ; CXCL12 ; Forkhead Box Protein M1 ; Forkhead Transcription Factors - biosynthesis ; FOXM1 ; Gene Expression Regulation, Neoplastic ; Glioblastoma ; Glioblastoma - pathology ; Humans ; Invasion ; Neoplasm Invasiveness - physiopathology ; Phosphatidylinositol 3-Kinases - physiology ; Proto-Oncogene Proteins c-akt - physiology ; Receptors, CXCR4 - biosynthesis ; Receptors, CXCR4 - metabolism ; RNA, Small Interfering - pharmacology ; Signal Transduction - physiology ; Up-Regulation</subject><ispartof>Biochemical and biophysical research communications, 2014-04, Vol.447 (1), p.1-6</ispartof><rights>2014 Elsevier Inc.</rights><rights>Copyright © 2014 Elsevier Inc. 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Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor; it is highly aggressive and is associated with a poor prognosis. Binding of the chemokine CXCL12 to its receptors (CXCR4 and CXCR7) contributes to the activation of many downstream signaling pathways and promotes the invasion of various malignant tumor cells, including GBM cells. FOXM1, a transcription factor involved in cell cycle regulation, is overexpressed in GBM and is involved in GBM progression. However, the molecular mechanisms by which CXCL12 promotes the invasion of human GBM cells remain unclear. In this study, we demonstrate that CXCL12 increases the production of FOXM1 by binding to CXCR4 in GBM cell lines. Furthermore, pretreatment with an inhibitor of the PI3K/AKT pathway abrogated the CXCL12-induced expression of FOXM1. In addition, there was a positive correlation between CXCL12/CXCR4 expression and FOXM1 expression in human malignant glioma tissues. Finally, a functional assay revealed that CXCL12 does not stimulate GBM cell invasion when FOXM1 expression is silenced using a small interfering RNA (siRNA). 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Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor; it is highly aggressive and is associated with a poor prognosis. Binding of the chemokine CXCL12 to its receptors (CXCR4 and CXCR7) contributes to the activation of many downstream signaling pathways and promotes the invasion of various malignant tumor cells, including GBM cells. FOXM1, a transcription factor involved in cell cycle regulation, is overexpressed in GBM and is involved in GBM progression. However, the molecular mechanisms by which CXCL12 promotes the invasion of human GBM cells remain unclear. In this study, we demonstrate that CXCL12 increases the production of FOXM1 by binding to CXCR4 in GBM cell lines. Furthermore, pretreatment with an inhibitor of the PI3K/AKT pathway abrogated the CXCL12-induced expression of FOXM1. In addition, there was a positive correlation between CXCL12/CXCR4 expression and FOXM1 expression in human malignant glioma tissues. 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subjects Astrocytoma - pathology
Brain Neoplasms - metabolism
Brain Neoplasms - pathology
Cell Line, Tumor
Chemokine
Chemokine CXCL12 - biosynthesis
CXCL12
Forkhead Box Protein M1
Forkhead Transcription Factors - biosynthesis
FOXM1
Gene Expression Regulation, Neoplastic
Glioblastoma
Glioblastoma - pathology
Humans
Invasion
Neoplasm Invasiveness - physiopathology
Phosphatidylinositol 3-Kinases - physiology
Proto-Oncogene Proteins c-akt - physiology
Receptors, CXCR4 - biosynthesis
Receptors, CXCR4 - metabolism
RNA, Small Interfering - pharmacology
Signal Transduction - physiology
Up-Regulation
title CXCL12-induced upregulation of FOXM1 expression promotes human glioblastoma cell invasion
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