1. CCR6 promotes tumor angiogenesis via the AKT/NF-κB/VEGF pathway in colorectal cancer.
- Author
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Zhu CC, Chen C, Xu ZQ, Zhao JK, Ou BC, Sun J, Zheng MH, Zong YP, and Lu AG
- Subjects
- Aged, Animals, Cell Line, Tumor, Cell Movement, Cell Proliferation, Disease Progression, Extracellular Matrix metabolism, Female, Gene Expression Regulation, Neoplastic, HCT116 Cells, HT29 Cells, Human Umbilical Vein Endothelial Cells, Humans, Male, Mice, Mice, Inbred BALB C, Mice, Nude, Middle Aged, Colorectal Neoplasms metabolism, NF-kappa B metabolism, Neovascularization, Pathologic, Proto-Oncogene Proteins c-akt metabolism, Receptors, CCR6 metabolism, Vascular Endothelial Growth Factor A metabolism
- Abstract
Chemokines and chemokine receptors play an important role in tumorigenesis. Angiogenesis is a vital part of the occurrence, development and metastasis of cancer. CCR6 is an important factor during tumor progression; however, its function in tumor angiogenesis is not fully understood. In our study, we found that CCR6 was significantly overexpressed in colorectal cancer (CRC) tissues and predicted a poor prognosis in CRC patients. We then verified the function of CCR6 on tumor angiogenesis in vivo and in vitro. We observed that silencing CCR6 could decrease angiogenesis by inhibiting the proliferation and migration of human umbilical vein endothelial cells (HUVECs), whereas overexpression of CCR6 can promote angiogenesis. Additionally, we investigated the molecular mechanisms and demonstrated that activation of the AKT/NF-κB pathway maybe involved in CCR6-mediated tumor angiogenesis, which was able to promote the secretion of vascular endothelial growth factor A (VEGF-A). In conclusion, CCR6 facilitates tumor angiogenesis via the AKT/NF-κB/VEGF pathway in colorectal cancer. CCR6 inhibition may be a novel option for anti-vascular treatment in CRC., (Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.)
- Published
- 2018
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