Selective suppression of nuclear retinoic acid receptor beta gene expression in human pancreatic carcinomas
- X Xu
- U Stier
- S Rosewicz
- A ElNaggar
- R Lotan
Affiliations: UNIV TEXAS, MD ANDERSON CANC CTR, DEPT TUMOR BIOL, HOUSTON, TX 77030 USA. UNIV TEXAS, MD ANDERSON CANC CTR, DEPT PATHOL, HOUSTON, TX 77030 USA. FREE UNIV BERLIN, KLINIKUM BENJAMIN FRANKLIN, DEPT INTERNAL MED, D-12200 BERLIN, GERMANY.
- Published online on: March 1, 1996 https://doi.org/10.3892/ijo.8.3.445
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Retinoids restore normal cell growth and differentiation in malignant cells and are considered as potential therapeutic agents. Before using retinoids for the treatment of pancreatic cancer it is important to determine the expression of nuclear retinoid receptors, which mediate most actions of retinoids on gene expression in normal and malignant tissues. Digoxigenin-labeled antisense riboprobes of retinoic acid receptors (RARs) alpha, beta, and gamma, and retinoid X receptor (RXR) alpha were used for in situ hybridization to histological sections of-specimens from 24 human pancreatic carcinomas, 20 of which also contained adjacent normal tissue. All four receptors were detected in adjacent normal pancreatic tissue specimens and RAR-alpha, RAR-gamma, and RXR-alpha were also detected in all pancreatic carcinoma specimens. In contrast, RAR-beta mRNA transcripts were detected in only 67% of the malignant tissues and when expressed, the level of expression was significantly lower than that of the corresponding adjacent normal tissues. Decreased RAR-beta gene expression was especially noted in moderately- and poorly-differentiated cancers. These findings suggest that selective decrease or lass of RAR-beta gene expression in certain pancreatic carcinomas in vivo might be associated with the development or progression of pancreatic cancer.