NDLI: CD105 promotes hepatocarcinoma cell invasion and metastasis through VEGF.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Li, Yan Zhai, Zhenhua Liu, Dan Zhong, Xinping Meng, Xin Yang, Qingquan Liu, Jingang Li, Hangyu
Description	Country affiliation: China Author Affiliation: Li Y ( Department of General Surgery, Affiliated Shengjing Hospital, China Medical University, Shenyang, China.)
Abstract	Hepatocellular carcinoma (HCC) is a leading cause of cancer-related morbidity and mortality. Tumor neovascularization is necessarily required for tumor progression and metastasis. CD105 and vascular endothelial growth factor (VEGF) have separately been identified as important contributors to angiogenesis; however, it is unclear if these factors interact to promote the progression of HCC. The goal of this study was to determine the interaction between CD105 and VEGF in HCC, using HCC tissue samples and the human HCC cell line SMMC-7721. In a survey of 89 HCC tumor samples, we determined that CD105 and VEGF expressions were positively correlated with each other and expressed at a higher level in tumor cells. Furthermore, the expression of CD105 was closely related to the tumor-node-metastasis (TNM) staging of HCC, degree of tumor differentiation, portal vein invasion, and lymph node metastasis (P < 0.05). Next, we used a lentiviral system to stably overexpress CD105 in SMMC-7721 cells, which was confirmed at the messenger RNA (mRNA) and protein level. We observed that VEGF expression was increased in these cells, as was cell motility and migration, as assessed using a wound healing assay and Transwell chamber system, respectively. Using VEGF small interfering RNA (siRNA), we also demonstrated that elevated VEGF expression is required to promote increased cell motility and migration in CD105-overexpressing cells. In conclusion, we interpret our data to prove that CD105 promotes the invasion and metastases of liver cancer cells by increasing VEGF expression. These results provide a new theoretical and experimental basis for the treatment of liver cancer.
File Format	HTM / HTML
ISSN	10104283
Issue Number	2
Volume Number	36
e-ISSN	14230380
Journal	Tumor Biology
Language	English
Publisher	Springer
Publisher Date	2015-02-01
Publisher Place	Netherlands
Access Restriction	Subscribed
Subject Keyword	Discipline Medicine__semicolon__oncology Antigens, Cd Biosynthesis Carcinoma, Hepatocellular Genetics Liver Neoplasms Receptors, Cell Surface Vascular Endothelial Growth Factor A Aged Aged, 80 And Over Pathology Disease Progression Female Gene Expression Regulation, Neoplastic Humans Male Middle Aged Neoplasm Invasiveness Neoplasm Metastasis Neoplasm Staging Neovascularization, Pathologic Prognosis Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Medicine Cancer Research

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