Stanniocalcin-1 promotes tumor angiogenesis through up-regulation of VEGF in gastric cancer cells

<p>Abstract</p> <p>Background</p> <p>Stanniocalcin-1(STC-1) is up-regulated in several cancers including gastric cancer. Evidences suggest that STC-1 is associated with carcinogenesis and angiogenic process. However, it is unclear on the exact role for STC-1 in inducing...

Full description

Bibliographic Details
Main Authors: Yu Li-ke, Huang Ya-hong, Zhao Guang-feng, Gao Qian-ying, Wang Ting-ting, He Ling-fang, Hou Ya-yi
Format: Article
Language:English
Published: BMC 2011-06-01
Series:Journal of Biomedical Science
Subjects:
Online Access:http://www.jbiomedsci.com/content/18/1/39
Description
Summary:<p>Abstract</p> <p>Background</p> <p>Stanniocalcin-1(STC-1) is up-regulated in several cancers including gastric cancer. Evidences suggest that STC-1 is associated with carcinogenesis and angiogenic process. However, it is unclear on the exact role for STC-1 in inducing angiogenesis and tumorigeneisis.</p> <p>Method</p> <p>BGC/STC cells (high-expression of STC-1) and BGC/shSTC cells (low- expression of STC-1) were constructed to investigate the effect of STC-1 on the xenograft tumor growth and angiogenesis <it>in vitro </it>and <it>in vivo</it>. ELISA assay was used to detect the expression of vascular endothelial growth factor (VEGF) in the supernatants. Neutralizing antibody was used to inhibit VEGF expression in supernatants. The expression of phosphorylated -PKCβII, phosphorylated -ERK1/2 and phosphorylated -P38 in the BGC treated with STC-1protein was detected by western blot.</p> <p>Results</p> <p>STC-1 could promote angiogenesis <it>in vitro </it>and <it>in vivo</it>, and the angiogenesis was consistent with VEGF expression <it>in vitro</it>. Inhibition of VEGF expression in supernatants with neutralizing antibody markedly abolished angiogenesis induced by STC-1 <it>in vitro</it>. The process of STC-1-regulated VEGF expression was mediated via PKCβII and ERK1/2.</p> <p>Conclusions</p> <p>STC-1 promotes the expression of VEGF depended on the activation of PKCβII and ERK1/2 pathways. VEGF subsequently enhances tumor angiogenesis which in turn promotes the gastric tumor growth.</p>
ISSN:1021-7770
1423-0127