学科主题基础医学
CMTM3, Located at the Critical Tumor Suppressor Locus 16q22.1, Is Silenced by CpG Methylation in Carcinomas and Inhibits Tumor Cell Growth through Inducing Apoptosis
Wang, Yu3; Li, Jisheng1,2; Cui, Yan1,2; Li, Ting3; Ng, Ka Man1,2; Geng, Hua1,2; Li, Henan3; Shu, Xing-sheng1,2; Li, Hongyu1,2; Liu, Wei3; Luo, Bing4; Zhang, Qian5,6; Mok, Tony Shu Kam1,2; Zheng, Wei7; Qiu, Xiaoyan3; Srivastava, Gopesh8; Yu, Jun9; Sung, Joseph J. Y.9; Chan, Anthony T. C.1,2; Ma, Dalong3; Tao, Qian1,2; Han, Wenling3
刊名CANCER RESEARCH
2009-06-15
DOI10.1158/0008-5472.CAN-08-3694
69期:12页:5194-5201
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology
研究领域[WOS]Oncology
关键词[WOS]STRESS-RESPONSIVE GENE ; CANCER ; EXPRESSION ; LINES ; DEATH ; HYPERMETHYLATION ; NASOPHARYNGEAL ; MALIGNANCIES ; MECHANISMS ; ESOPHAGEAL
英文摘要

Closely located at the tumor suppressor locus 16q22.1, CKLF-like MARVEL transmembrane domain-containing member 3 and 4 (CMTM3 and CMTM4) encode two CMTM family proteins, which link chemokines and the transmembrane-4 superfamily. In contrast to the broad expression of both CMTM3 and CMTM4 in normal human adult tissues, only CMTM3 is silenced or down-regulated in common carcinoma (gastric, breast, nasopharyngeal, esophageal, and colon) cell lines and primary tumors. CMTM3 methylation was not detected in normal epithelial cell lines and tissues, with weak methylation present in only 5 of 35 (14%) gastric cancer adjacent normal tissues. Furthermore, immunohistochemistry showed that CMTM3 protein was absent in 12 of 35 (34%) gastric and I of 2 colorectal tumors, which was well correlated with its methylation status. The silencing of CMTM3 is due to aberrant promoter CpG methylation that could be reversed by pharmacologic demethylation. Ectopic expression of CMTM3 strongly suppressed the colony formation of carcinoma cell lines. In addition, CMTM3 inhibited tumor cell growth and induced apoptosis with caspase-3 activation. Thus CMTM3 exerts tumor-suppressive functions in tumor cells: with frequent epigenetic inactivation by promoter CpG methylation in common carcinomas. [Cancer Res 2009;69(12):5194-201]

语种英语
WOS记录号WOS:000267506400035
项目编号NCET-07-0013 ; 2006AA02A305 ; CA06/07.SC03
资助机构New Century Excellent Talents in University ; China High Tech 863 Program ; Michael and Betty Kadoorie Cancer Genetics Research Program ; Hong Kong RGC Central Allocation
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被引频次:62[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/67799
专题北京大学基础医学院_北京大学人类疾病基因研究中心
北京大学基础医学院
北京大学第二临床医学院_检验科
作者单位1.Gen Hosp Peoples Liberat Army, Dept Gen Surg, Beijing, Peoples R China
2.Peking Univ, Dept Urol, Hosp 1, Beijing 100871, Peoples R China
3.Peking Univ, Inst Urol, Beijing 100871, Peoples R China
4.Chinese Univ Hong Kong, Dept Clin Oncol, Canc Epigenet Lab,Hong Kong Canc Inst, State Key Lab Oncol S China,Sir YK Pao Ctr Canc, Shatin, Hong Kong, Peoples R China
5.Chinese Univ Hong Kong, Li Ka Shing Inst Hlth Sci, Shatin, Hong Kong, Peoples R China
6.Peking Univ, Ctr Human Dis Genom, Dept Immunol, Hlth Sci Ctr, Beijing 100871, Peoples R China
7.Chinese Univ Hong Kong, Inst Digest Dis, Dept Med & Therapeut, Shatin, Hong Kong, Peoples R China
8.Univ Hong Kong, Hong Kong Special Adm Reg, Dept Pathol, Hong Kong, Hong Kong, Peoples R China
9.Qingdao Univ, Coll Med, Dept Med Microbiol, Qingdao 266071, Peoples R China
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Wang, Yu,Li, Jisheng,Cui, Yan,et al. CMTM3, Located at the Critical Tumor Suppressor Locus 16q22.1, Is Silenced by CpG Methylation in Carcinomas and Inhibits Tumor Cell Growth through Inducing Apoptosis[J]. CANCER RESEARCH,2009,69(12):5194-5201.
APA Wang, Yu.,Li, Jisheng.,Cui, Yan.,Li, Ting.,Ng, Ka Man.,...&Han, Wenling.(2009).CMTM3, Located at the Critical Tumor Suppressor Locus 16q22.1, Is Silenced by CpG Methylation in Carcinomas and Inhibits Tumor Cell Growth through Inducing Apoptosis.CANCER RESEARCH,69(12),5194-5201.
MLA Wang, Yu,et al."CMTM3, Located at the Critical Tumor Suppressor Locus 16q22.1, Is Silenced by CpG Methylation in Carcinomas and Inhibits Tumor Cell Growth through Inducing Apoptosis".CANCER RESEARCH 69.12(2009):5194-5201.
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