Dopamine agonist resistance-related endocan promotes angiogenesis and cells viability of prolactinomas

doi:10.1007/s12020-015-0824-2

科研成果详情

题名	Dopamine agonist resistance-related endocan promotes angiogenesis and cells viability of prolactinomas
作者	Cai, Lin1; Leng, Zhi Gen 1; Guo, Yu Hang 1; Lin, Shao Jian 2; Wu, Ze Rui 1; Su, Zhi Peng 1; Lu, Jiang Long 1; Wei, Li Fei 1; Zhuge, Qi Chuan 1; Jin, Kunlin 3; Wu, Zhe Bao 1,2
发表日期	2016-06
发表期刊	ENDOCRINE 影响因子和分区
语种	英语
原始文献类型	Article
关键词	Prolactinoma Endocan Dopamine agonist Bromocriptine Angiogenesis Endothelial cell-specific molecule 1
其他关键词	HEPATOCELLULAR-CARCINOMA ; ENDOTHELIAL MARKERS ; MICROVESSEL DENSITY ; MICROARRAY ANALYSIS ; PITUITARY-ADENOMAS ; VASCULAR ENDOCAN ; CAVERNOUS SINUS ; LUNG-CANCER ; FOLLOW-UP ; IN-VITRO
摘要	Dopamine agonists (DAs) are the first-line treatment of prolactinomas. They function through the dopamine 2 receptor (D2R) in the tumor cells. Endocan, also called endothelial cell-specific molecule-1 (ESM1), has been described as a marker of neoangiogenesis. However, whether ESM1 promotes the resistance of prolactinomas to DA therapy is largely unknown. In our study, 25 patients with prolactinomas were divided into resistant- and sensitive- groups according to the clinical response to bromocriptine. We found that ESM1-microvessel density of resistant prolactinomas was significantly higher than that of sensitive prolactinomas (47.9 +/- 11.6, n = 8, vs 13.1 +/- 2.8, n = 17, p = 0.0006), indicating that ESM1 was a DA resistance-related gene. Immunostaining showed that ESM1 was expressed in tumor vessels and sporadic tumor cells, and ESM1 was overlapped with the Smooth Muscle Actin (SMA) and von Willebrand Factor (VWF) in the tumor vessels. Silencing of ESM1 markedly suppressed the viability of GH3 and MMQ cells in vitro, and furthermore, significantly increased the sensitivity of GH3 and MMQ cells to DA treatment. Additionally, silencing of ESM1 down-regulated the angiogenesis-associated genes, such as VEGFR2, FGF2, CD34, CD31, VWF, and EGFR. Knockdown of ESM1 decreased endothelial tube formation of HUVECs, and significantly increased the sensitivity of HUVECs to Avastin treatment. Therefore, we first demonstrate that DA resistance-related ESM1 promotes the angiogenesis and tumor cells growth of prolactinomas, suggesting that ESM1 may be a novel therapeutic target for prolactinomas.
资助项目	National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81271523, 81471392]; Zhejiang Open Foundation of the Top Key Discipline [LKYJ015]
出版者	SPRINGER
出版地	NEW YORK
ISSN	1355-008X
EISSN	1559-0100
卷号	52 期号:3 页码:641-651
DOI	10.1007/s12020-015-0824-2
页数	11
WOS类目	Endocrinology & Metabolism
WOS研究方向	Endocrinology & Metabolism
WOS记录号	WOS:000376668100026
收录类别	SCIE ; PUBMED ; SCOPUS
URL	查看原文
PubMed ID	26662185
SCOPUSEID	2-s2.0-84949636903
通讯作者地址	[Wu, Zhe Bao]Department of Neurosurgery,First Affiliated Hospital of Wenzhou Medical University,Wenzhou,325000,China
Scopus学科分类	Endocrinology, Diabetes and Metabolism;Endocrinology
引用统计	被引频次：12[WOS] [WOS记录] [WOS相关记录]
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/8723
专题	附属第一医院
通讯作者	Wu, Zhe Bao
作者单位	1.Department of Neurosurgery,First Affiliated Hospital of Wenzhou Medical University,Wenzhou,325000,China; 2.Department of Neurosurgery,Ruijin Hospital,Shanghai Jiao Tong University School of Medicine,200025,Shanghai,China; 3.Department of Pharmacology and Neuroscience,University of North Texas Health Science Center,Fort Worth,76107,United States
第一作者单位	附属第一医院
通讯作者单位	附属第一医院
第一作者的第一单位	附属第一医院
推荐引用方式 GB/T 7714	Cai, Lin,Leng, Zhi Gen,Guo, Yu Hang,et al. Dopamine agonist resistance-related endocan promotes angiogenesis and cells viability of prolactinomas[J]. ENDOCRINE,2016,52(3):641-651.
APA	Cai, Lin., Leng, Zhi Gen., Guo, Yu Hang., Lin, Shao Jian., Wu, Ze Rui., ... & Wu, Zhe Bao. (2016). Dopamine agonist resistance-related endocan promotes angiogenesis and cells viability of prolactinomas. ENDOCRINE, 52(3), 641-651.
MLA	Cai, Lin,et al."Dopamine agonist resistance-related endocan promotes angiogenesis and cells viability of prolactinomas".ENDOCRINE 52.3(2016):641-651.