Factor inhibiting HIF1 alpha (FIH-1) functions as a tumor suppressor in human colorectal cancer by repressing HIF1 alpha pathway

doi:10.1080/15384047.2014.1002346

科研成果详情

题名	Factor inhibiting HIF1 alpha (FIH-1) functions as a tumor suppressor in human colorectal cancer by repressing HIF1 alpha pathway
作者	Chen, Tao 1; Ren, Zhong 1; Ye, Le-Chi3; Zhou, Ping-Hong 1; Xu, Jian-Min 2; Shi, Qiang 1; Yao, Li-Qing 1; Zhong, Yun-Shi 1
发表日期	2015-02
发表期刊	CANCER BIOLOGY & THERAPY 影响因子和分区
语种	英语
原始文献类型	Article
关键词	colorectal cancer FIH-1 HIF1 pathway prognosis progression tumor suppressor tumorigenesis
其他关键词	HYPOXIA-INDUCIBLE FACTOR ; TRANSCRIPTIONAL ACTIVITY ; REGULATORY FACTOR ; GENETIC-ANALYSIS ; HIF PATHWAY ; HIF-1-ALPHA ; EXPRESSION ; CARCINOMA ; GROWTH ; PHD-2
摘要	Colorectal cancer (CRC) is one of the most common cancers worldwide. The molecular mechanisms underlying CRC development involve a multistep process with the accumulation of both genetic and epigenetic changes. To deeply understand CRC tumorigenesis and progression, advances in identification of novel mechanisms and key factors are therefore in an urgent need. Here, we examined the correlation of factor inhibiting HIF-1 (FIH-1) expression with clinicopathological features of CRC. The finding that FIH-1 was not only significantly decreased in tumor tissue but also was significantly correlated with tumor invading depth, lymph node involvement, and metastasis suggested the role of FIH-1 as a tumor suppressor in CRC development. To further support the above hypothesis, we performed both in vitro and in vivo experiments to identify the role of FIH-1 in CRC development. FIH-1 was found to inhibit CRC cell proliferation, migration, invasion, and colony formation in vitro. FIH-1 was also shown to repress LOVO xenograft tumor growth in vivo. To decipher the mechanism, we examined the expression level of HIF-1 and its target genes. We found that FIH-1 was able to inhibit HIF1 mediated transcription of GLUT1 and VEGF in CRC cells. The above observation points to the possibility that loss or decreased expression of FIH-1 gene may lead to a constitutive activation of HIF1 and an alteration of HIF-1 targets such as GLUT-1 and VEGF. These findings highlight the critical role of FIH-1 in CRC and indicate FIH-1 functions as a tumor suppressor in human CRC by repressing HIF1 pathway.
资助项目	National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81101566]; Scientific Funds of Shanghai Government [12QA1400600, XYQ2011017, 2013SY045, 2013SY054, 11411950500, 11411950501, 13411951600, 201305]
出版者	TAYLOR & FRANCIS INC
出版地	PHILADELPHIA
ISSN	1538-4047
EISSN	1555-8576
卷号	16 期号:2 页码:244-252
DOI	10.1080/15384047.2014.1002346
页数	9
WOS类目	Oncology
WOS研究方向	Oncology
WOS记录号	WOS:000351631200012
收录类别	SCIE ; SCOPUS
URL	查看原文
Pubmed记录号	25602156
Scopus记录号	2-s2.0-84924545752
通讯作者地址	[Yao, Li-Qing]Endoscopy Center,Zhongshan Hospital of Fudan University,Shanghai,China
scopus学科分类	Molecular Medicine;Oncology;Pharmacology;Cancer Research
引用统计	被引频次：24[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/17352
专题	附属第一医院_肿瘤外科
通讯作者	Yao, Li-Qing
作者单位	1.Endoscopy Center,Zhongshan Hospital of Fudan University,Shanghai,China; 2.Department of General Surgery,Zhongshan Hospital of Fudan University,Shanghai,China; 3.Department of Oncological Surgery,First Affiliated Hospital of Wenzhou Medical University,Wenzhou,China
推荐引用方式 GB/T 7714	Chen, Tao,Ren, Zhong,Ye, Le-Chi,et al. Factor inhibiting HIF1 alpha (FIH-1) functions as a tumor suppressor in human colorectal cancer by repressing HIF1 alpha pathway[J]. CANCER BIOLOGY & THERAPY,2015,16(2):244-252.
APA	Chen, Tao., Ren, Zhong., Ye, Le-Chi., Zhou, Ping-Hong., Xu, Jian-Min., ... & Zhong, Yun-Shi. (2015). Factor inhibiting HIF1 alpha (FIH-1) functions as a tumor suppressor in human colorectal cancer by repressing HIF1 alpha pathway. CANCER BIOLOGY & THERAPY, 16(2), 244-252.
MLA	Chen, Tao,et al."Factor inhibiting HIF1 alpha (FIH-1) functions as a tumor suppressor in human colorectal cancer by repressing HIF1 alpha pathway".CANCER BIOLOGY & THERAPY 16.2(2015):244-252.