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• W2040707218 abstract "No AccessJournal of UrologyInvestigative Urology1 Aug 2010Aberrant Promoter Methylation of DLEC1, a Critical 3p22 Tumor Suppressor for Renal Cell Carcinoma, is Associated With More Advanced Tumor Stage Qian Zhang, Jianming Ying, Jisheng Li, Yichao Fan, Fan Fong Poon, Ka Man Ng, Qian Tao, and Jie Jin Qian ZhangQian Zhang Department of Urology, Peking University First Hospital and Institute of Urology, Peking University, China National Research Center for Genitourinary Oncology, China Joint Center for Cancer Epigenetics, China Equal study contribution. More articles by this author , Jianming YingJianming Ying National Research Center for Genitourinary Oncology, China Joint Center for Cancer Epigenetics, China Department of Pathology, Cancer Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China Equal study contribution. More articles by this author , Jisheng LiJisheng Li Cancer Epigenetics Laboratory, State Key Laboratory in Oncology in South China, Sir Y. K. Pao Center for Cancer, Department of Clinical Oncology, Hong Kong Cancer Institute and Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong Special Administrative Region, People's Republic of China More articles by this author , Yichao FanYichao Fan Cancer Epigenetics Laboratory, State Key Laboratory in Oncology in South China, Sir Y. K. Pao Center for Cancer, Department of Clinical Oncology, Hong Kong Cancer Institute and Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong Special Administrative Region, People's Republic of China More articles by this author , Fan Fong PoonFan Fong Poon Cancer Epigenetics Laboratory, State Key Laboratory in Oncology in South China, Sir Y. K. Pao Center for Cancer, Department of Clinical Oncology, Hong Kong Cancer Institute and Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong Special Administrative Region, People's Republic of China More articles by this author , Ka Man NgKa Man Ng Cancer Epigenetics Laboratory, State Key Laboratory in Oncology in South China, Sir Y. K. Pao Center for Cancer, Department of Clinical Oncology, Hong Kong Cancer Institute and Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong Special Administrative Region, People's Republic of China More articles by this author , Qian TaoQian Tao National Research Center for Genitourinary Oncology, China Joint Center for Cancer Epigenetics, China Cancer Epigenetics Laboratory, State Key Laboratory in Oncology in South China, Sir Y. K. Pao Center for Cancer, Department of Clinical Oncology, Hong Kong Cancer Institute and Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong Special Administrative Region, People's Republic of China More articles by this author , and Jie JinJie Jin Department of Urology, Peking University First Hospital and Institute of Urology, Peking University, China National Research Center for Genitourinary Oncology, China Joint Center for Cancer Epigenetics, China More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2010.03.108AboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract Purpose: Identifying tumor suppressor genes silenced by promoter CpG methylation uncovers mechanisms of tumorigenesis and identifies new epigenetic biomarkers for early cancer detection. DLEC1 is located at 3p22.3, a critical tumor suppressor gene locus for renal cell carcinoma. We explored its epigenetic alteration in renal cell carcinoma and possible clinicopathological association. Materials and Methods: We examined DLEC1 expression and methylation by semiquantitative reverse transcriptase and methylation specific polymerase chain reaction in 9 renal cell carcinoma cell lines and 81 primary tumors. We also analyzed the relationship between DLEC1 methylation and clinicopathological features in patients with renal cell carcinoma. We assessed DLEC1 inhibition of renal cell carcinoma cell growth by colony formation assay. Results: DLEC1 methylation and down-regulation were detected in all renal cell carcinoma cell lines. Treatment with 5-aza-2′-deoxycytidine (Sigma®) and/or trichostatin A (Cayman Chemical, Ann Arbor, Michigan) reversed methylation and restored DLEC1 expression, indicating that methylation directly mediates its silencing. Aberrant methylation was further detected in 25 of 81 primary tumors (31%) but only 1 of 53 nonmalignant renal tissues (2%) showed methylation. DLEC1 methylation status was significantly associated with TNM classification and grade in patients with renal cell carcinoma (chi-square test p = 0.01 and 0.04, respectively). DLEC1 ectopic expression in silenced renal cell carcinoma cells resulted in substantial tumor cell clonogenicity inhibition. Conclusions: To our knowledge we report for the first time that DLEC1 is often down-regulated by CpG methylation and shows tumor inhibitory function in renal cell carcinoma cells, indicating its role as a tumor suppressor. DLEC1 tumor specific methylation may serve as a biomarker for early detection and prognosis prediction of this tumor. References 1 : Epidemiologic aspects of renal cell carcinoma. Semin Oncol2006; 33: 527. Google Scholar 2 : Two genetic hits (more or less) to cancer. Nat Rev Cancer2001; 1: 157. 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Google Scholar 9 : Epigenetic inactivation of the candidate tumor suppressor gene HOXB13 in human renal cell carcinoma. Oncogene2006; 25: 1733. Google Scholar 10 : Loss of heterozygosity and methylation of p16 in renal cell carcinoma. Urol Res2003; 31: 159. Google Scholar 11 : Aberrant methylation of the 8p22 tumor suppressor gene DLC1 in renal cell carcinoma. Cancer Lett2007; 249: 220. Google Scholar 12 : Search for unknown tumor-antagonizing genes. Genes Chromosomes Cancer2003; 38: 307. Google Scholar 13 : Frequent inactivation of RASSF1A, BLU, and SEMA3B on 3p21 3 by promoter hypermethylation and allele loss in non-small cell lung cancer. Cancer Lett2005; 225: 131. Google Scholar 14 : The tumor suppressor gene DLEC1 is frequently silenced by DNA methylation in hepatocellular carcinoma and induces G1 arrest in cell cycle. J Hepatol2008; 48: 433. Google Scholar 15 : DLEC1 is a functional 3p22.3 tumour suppressor silenced by promoter CpG methylation in colon and gastric cancers. Br J Cancer2009; 100: 663. Google Scholar 16 : American Joint Committee on Cancer Staging Manual. New York: Springer-Verlag2002. Google Scholar 17 : The stress-responsive gene GADD45G is a functional tumor suppressor, with its response to environmental stresses frequently disrupted epigenetically in multiple tumors. Clin Cancer Res2005; 11: 6442. Google Scholar 18 : Defective de novo methylation of viral and cellular DNA sequences in ICF syndrome cells. Hum Mol Genet2002; 11: 2091. Google Scholar 19 : Candidate tumor-suppressor gene DLEC1 is frequently downregulated by promoter hypermethylation and histone hypoacetylation in human epithelial ovarian cancer. Neoplasia2006; 8: 268. Google Scholar 20 : Epigenetic inactivation of the deleted in lung and esophageal cancer 1 gene in nasopharyngeal carcinoma. Genes Chromosomes Cancer2007; 46: 171. Google Scholar 21 : Promoter hypermethylation profile of kidney cancer. Clin Cancer Res2004; 10: 3972. Google Scholar 22 : Molecular cloning of a candidate tumor suppressor gene, DLC1, from chromosome 3p21 3. Cancer Res1999; 59: 1966. Google Scholar 23 : The Mayo Clinic experience with surgical management, complications and outcome for patients with renal cell carcinoma and venous tumour thrombus. BJU Int2004; 94: 33. Google Scholar 24 : Gene methylation and early detection of genitourinary cancer: the road ahead. Nat Rev Cancer2007; 7: 531. Google Scholar 25 : Quantitative detection of promoter hypermethylation of multiple genes in the tumor, urine, and serum DNA of patients with renal cancer. Cancer Res2004; 64: 5511. Google Scholar © 2010 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 184Issue 2August 2010Page: 731-737 Advertisement Copyright & Permissions© 2010 by American Urological Association Education and Research, Inc.Keywordsgenes, tumor suppressormethylationcarcinoma, renal cellDLEC1 (deleted in lung cancer) protein, humankidneyAcknowledgmentsCell lines were provided by Drs. Shuen-Kuei Liao, Chang Gung University, Taiwan, Republic of China, and Johng S. Rhim, Center for Prostate Disease Research, Uniformed Services University of the Health Sciences, Bethesda, Maryland, or obtained from ATCC®. Ada Ho Yan Wong provided technical support.MetricsAuthor Information Qian Zhang Department of Urology, Peking University First Hospital and Institute of Urology, Peking University, China National Research Center for Genitourinary Oncology, China Joint Center for Cancer Epigenetics, China Equal study contribution. More articles by this author Jianming Ying National Research Center for Genitourinary Oncology, China Joint Center for Cancer Epigenetics, China Department of Pathology, Cancer Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China Equal study contribution. More articles by this author Jisheng Li Cancer Epigenetics Laboratory, State Key Laboratory in Oncology in South China, Sir Y. K. Pao Center for Cancer, Department of Clinical Oncology, Hong Kong Cancer Institute and Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong Special Administrative Region, People's Republic of China More articles by this author Yichao Fan Cancer Epigenetics Laboratory, State Key Laboratory in Oncology in South China, Sir Y. K. Pao Center for Cancer, Department of Clinical Oncology, Hong Kong Cancer Institute and Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong Special Administrative Region, People's Republic of China More articles by this author Fan Fong Poon Cancer Epigenetics Laboratory, State Key Laboratory in Oncology in South China, Sir Y. K. Pao Center for Cancer, Department of Clinical Oncology, Hong Kong Cancer Institute and Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong Special Administrative Region, People's Republic of China More articles by this author Ka Man Ng Cancer Epigenetics Laboratory, State Key Laboratory in Oncology in South China, Sir Y. K. Pao Center for Cancer, Department of Clinical Oncology, Hong Kong Cancer Institute and Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong Special Administrative Region, People's Republic of China More articles by this author Qian Tao National Research Center for Genitourinary Oncology, China Joint Center for Cancer Epigenetics, China Cancer Epigenetics Laboratory, State Key Laboratory in Oncology in South China, Sir Y. K. Pao Center for Cancer, Department of Clinical Oncology, Hong Kong Cancer Institute and Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong Special Administrative Region, People's Republic of China More articles by this author Jie Jin Department of Urology, Peking University First Hospital and Institute of Urology, Peking University, China National Research Center for Genitourinary Oncology, China Joint Center for Cancer Epigenetics, China More articles by this author Expand All Advertisement PDF downloadLoading ..." @default.
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