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| E-CADHERIN EXPRESSION IS SILENCED BY DNA HYPERMETHYLATION IN HUMAN BREAST AND PROSTATE CARCINOMAS |
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| Author(s): GRAFF JR, HERMAN JG, LAPIDUS RG, CHOPRA H, XU R, JARRARD DF, ISAACS WB, PITHA PM, DAVIDSON NE, BAYLIN SB |
| Source: CANCER RESEARCH Volume: 55 Issue: 22 Pages: 5195-5199 Published: NOV 15 1995 |
| Times Cited: 497 References: 32 |
| Abstract: Expression of the Ca2+-dependent, homotypic cell:cell adhesion molecule, E-cadherin (E-cad), suppresses tumor cell invasion and metastasis in experimental tumor models. Decreased E-cad expression is common in poorly differentiated, advanced-stage carcinomas. These data implicate E-cad as an ''invasion suppressor'' gene. The mechanism by which E-cad is silenced in advanced stage carcinomas is unclear. In this report, we show that: (a) the 5' CpG island of E-cad is densely methylated in E-cad-negative breast and prostate carcinoma cell lines and primary breast carcinoma tissue but is unmethylated in normal breast tissue; (b) treatment with the demethylating agent, 5-aza-2'-deoxycytidine, partially restores E-cad RNA and protein levels in E-cad-negative breast and prostate carcinoma cell lines; and (c) an E-cad promoter/CAT construct is expressed in both E-cad-positive and -negative breast and prostate carcinoma cell lines, indicating that these cells have the active transcriptional machinery necessary for E-ead gene expression. Our data demonstrate that frequent loss of E-cad expression in human breast and prostate carcinomas results from hypermethylation of the E-cad promoter region. |
| Document Type: Note |
| Language: English |
Addresses:
1. JOHNS HOPKINS UNIV, CTR ONCOL, BALTIMORE, MD 21231 USA
2. JOHNS HOPKINS UNIV, MED CTR, BALTIMORE, MD 21231 USA |
| Publisher: AMER ASSOC CANCER RESEARCH, PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 |
| Subject Category: Oncology |
| IDS Number: TD887 |
| ISSN: 0008-5472 |
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| | | | | | | | | Record from Web of Science® | | | | | | | | | |