NDLI: IL-17 promotes tumor angiogenesis through Stat3 pathway mediated upregulation of VEGF in gastric cancer.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wu, Xiaoqin Yang, Tao Liu, Xiang Guo, Jia Nian Xie, Tingting Ding, Yuanwei Lin, Manpeng Yang, Hui
Description	Country affiliation: China Author Affiliation: Wu X ( Department of Gastroenterology, Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510182, China. wuxiaoqin150126@163.com.); Yang T ( Department of Gastroenterology, Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510182, China.); Liu X ( Department of Gastroenterology, Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510182, China.); Guo JN ( Department of Gastroenterology, Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510182, China.); Xie T ( Department of Gastroenterology, Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510182, China.); Ding Y ( Department of Gastroenterology, Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510182, China.); Lin M ( Department of Gastroenterology, Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510182, China.); Yang H ( Department of Gastroenterology, Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510182, China. yanghui150126@163.com.)
Abstract	Gastric cancer is the world's second most common malignancy and is a major threat to global health. IL-17, a CD4 T cell-derived mediator of angiogenesis, plays a major role in stimulating angiogenesis by regulating the production of a variety of proangiogenic factors, including the vascular endothelial growth factor (VEGF). The level of VEGF expression correlates with tumor progression and metastasis in gastric cancer tissues. Abnormal activation of signal transducer and activator of transcription 3 (Stat3) rendered the tumor cells highly angiogenic, which is manifested by an increased microvascular density (MVD) and considered it as a potential molecular marker for poor prognosis in gastric cancer angiogenesis. We determined that IL-17A-induced VEGF upregulation and neovascularization through a Stat3-mediated signaling pathway and hypothesized that blocking the Stat3 activation by using JSI-124, an inhibitor of phosphorylated Stat3, could significantly reduce the VEGF expression and can thus prevent angiogenesis. We showed an inhibition of angiogenesis and tumor progression when JSI-124 was treated with IL-17A in the cells and xenografts in an animal model and suggested that targeting the Stat pathway with JSI-124 could derive an effective therapeutic target for gastric cancers and could be a promising drug in gastric cancer treatment.
File Format	HTM / HTML
ISSN	10104283
Issue Number	4
Journal	Tumor Biology
Volume Number	37
e-ISSN	14230380
Language	English
Publisher	Springer
Publisher Date	2016-04-01
Publisher Place	Netherlands
Access Restriction	Subscribed
Content Type	Text
Resource Type	Article
Subject	Medicine Cancer Research

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