DCC promoter hypermethylation in esophageal squamous cell carcinoma

Hannah Lui Park, Sook Kim Myoung, Keishi Yamashita, William Westra, Andre Lopes Carvalho, Juna Lee, Wei Wen Jiang, Hyen Baek Jin, Junwei Liu, Motonobu Osada, Chul So Moon, Joseph A. Califano, Masaki Mori, David Sidransky

研究成果: Contribution to journalArticle査読

33 被引用数 (Scopus)

抄録

Deleted in Colorectal Cancer (DCC) is a putative tumor suppressor gene, whose loss has been implicated in colorectal tumorigenesis. Decreased or loss of DCC expression has been demonstrated in a number of human cancers, including esophageal cancer. In this study, we analyzed esophageal quamous cell carcinoma (ESCC) cell lines and primary ESCCs as well as normal esophageal tissues for DCC methylation by bisulfite sequencing, methylation-specific PCR (MSP) and/or quantitative methylation-specific PCR (qMSP). When a qMSP cut-off value for positivity was set to 1.0, DCC methylation was detected in 10 of 12 ESCC cell lines tested, 74% of primary ESCCs (n = 70), 0% of corresponding normal esophageal tissues (n = 20) and 0% of normal esophagus from healthy individuals (n = 19). DCC expression was undetectable in the majority of ESCC cell lines, and treatment with the DNA methyltransferase inhibitor 5-aza-2′- deoxycytidine reactivated gene expression. DCC overexpression suppressed colony formation in ESCC cell lines, suggesting that DCC may function as a tumor suppressor gene in the esophagus. However, DCC methylation was not associated with any clinical or pathologic parameters measured. We have demonstrated that DCC methylation is a frequent and cancer-specific event in primary ESCCs, suggesting that DCC and associated pathways may represent a new diagnostical therapeutic target.

本文言語英語
ページ(範囲)2498-2502
ページ数5
ジャーナルInternational Journal of Cancer
122
11
DOI
出版ステータス出版済み - 6 1 2008
外部発表はい

All Science Journal Classification (ASJC) codes

  • 腫瘍学
  • 癌研究

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