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DCC promoter hypermethylation in esophageal squamous cell carcinoma

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

Publisher
John Wiley and Sons
Year
2008
Tongue
French
Weight
220 KB
Volume
122
Category
Article
ISSN
0020-7136

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✦ Synopsis

Abstract

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 squamous 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. © 2008 Wiley‐Liss, Inc.

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