Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2018 Jan 2;36(1):10-18.
doi: 10.1080/07357907.2017.1422512. Epub 2018 Jan 30.

Knockdown of CXCR4 Inhibits CXCL12-Induced Angiogenesis in HUVECs through Downregulation of the MAPK/ERK and PI3K/AKT and the Wnt/β-Catenin Pathways

Affiliations

Knockdown of CXCR4 Inhibits CXCL12-Induced Angiogenesis in HUVECs through Downregulation of the MAPK/ERK and PI3K/AKT and the Wnt/β-Catenin Pathways

Zhi-Yu Song et al. Cancer Invest. .

Erratum in

  • Erratum.
    [No authors listed] [No authors listed] Cancer Invest. 2018 Jan 2;36(1):92. doi: 10.1080/07357907.2018.1438841. Cancer Invest. 2018. PMID: 29485345 No abstract available.

Abstract

CXCL12 is an extracellular chemokine binding to cell surface receptor CXCR4. We found that activation of CXCL12/CXCR4 axis stimulated angiogenesis in endothelial cells. Knockdown of CXCR4 in endothelial cells prevented the branch points of angiogenesis. Endothelial cells exposed to CXCL12 presented high level of epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), and matrix metalloproteinase MMP-2, but not in CXCR4 knockdown cells. Further studies revealed that activation of CXCL12/CXCR4 axis in vascular endothelial cells stimulates the angiogenesis through upregulation of the MAPK/ERK and PI3K/AKT and Wnt/β-catenin pathways. Conclusion, downregulation of CXCR4 could inhibit angiogenesis in cancer tissues.

Keywords: Angiogenesis; CXCR4/CXCL12 axis; MAPK/ERK; PI3K/AKT; Vascular endothelial cells; Wnt/β-catenin.

PubMed Disclaimer

MeSH terms

LinkOut - more resources