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http://dx.doi.org/10.7314/APJCP.2016.17.4.2217

VEGFR2 Expression in Head and Neck Squamous Cell Carcinoma Cancer Cells Mediates Proliferation and Invasion  

Xu, Hui-Min (Department of Otolaryngology-Head and Neck Surgery, Changshu No.1 People's Hospital Affiliated to Soochow University)
Zhu, Jian-Guo (Department of Otolaryngology-Head and Neck Surgery, Changshu No.1 People's Hospital Affiliated to Soochow University)
Gu, Lian (Department of Otolaryngology-Head and Neck Surgery, Changshu No.1 People's Hospital Affiliated to Soochow University)
Hu, Song-Qun (Department of Otolaryngology-Head and Neck Surgery, Affiliated Hospital of Nantong University)
Wu, Hao (Department of Otolaryngology-Head and Neck Surgery, Affiliated Hospital of Nantong University)
Publication Information
Asian Pacific Journal of Cancer Prevention / v.17, no.4, 2016 , pp. 2217-2221 More about this Journal
Abstract
Vascular endothelial growth factor 2 (VEGFR2) was initially identified as a receptor of VEGF on endothelial cells with a role in regulating angiogenesis during organism development and tumorigenesis. Previously, in cancer tissue, VEGFR2 has been reported to be expressed in endothelial cells. In our research, we found that VEGFR2 was expressed not only in endothelial cells but also cancer cells in head and neck squamous cell carcinomas (HNSCCs). Knockdown of VEGFR2 in Hep2 cells could arrest the cell cycle in G0/G1, leading to a decrease in proliferation. We also present evidence that MAPK/ERK signal pathways and expression of CDK1 downstream of VEGFR2 might regulate proliferation and cell cycle arrest. Furthermore, we discovered that down-regulate VEGRF2 in Hep2 cells could significantly affect the invasion ability. Taken together, our data suggest that VEGFR2 might regulate proliferation and invasion in HNSCC cancer cells in vivo.
Keywords
HNSCC; VEGFR2; proliferation; invasion;
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