Abstract
We recently observed that growth inhibition of esophageal cancer cells by retinoic acid (RA) was associated with both constitutive expression and RA-induced up-regulation of RA receptor beta (RAR-beta). Cell lines that did not express RAR-beta were also resistant to RA. To explore the expression of RAR-beta mRNA in vivo, we analyzed esophageal tissue specimens from 16 normal mucosae, 30 dysplastic lesions, and 157 esophageal tumors by in situ hybridization. RAR-beta was detected in 88% (14/16) of normal esophageal tissues and in 96% (96/100) of distant normal esophageal mucosa from cancer specimens. In contrast, RAR-beta was expressed in only 57% (17/30) of dysplastic lesions and in 54% (84/157) of carcinomas. Among esophageal carcinomas RAR-beta mRNA was expressed in 62% (26/42) of well-differentiated, 54% (27/50) of moderately differentiated, and only 29% (4/14) of poorly differentiated SCCs. Our data suggest that the loss of RAR-beta expression is an early event associated with esophageal carcinogenesis and the status of squamous differentiation.
MeSH Terms
Aged
Cell Differentiation/genetics
Esophageal Neoplasms/genetics,metabolism,pathology
Female
Gene Expression Regulation, Neoplastic
Humans
Immunohistochemistry
Male
Middle Aged
Receptors, Retinoic Acid/biosynthesis,genetics
Up-Regulation
Chemicals
Receptors, Retinoic Acid
retinoic acid receptor beta
Authors & Affiliations
7 authors, click to expand affiliations / ORCID
Qiu H
Departments of Clinical Cancer Prevention, Thoracic/Head and Neck Medical Oncology, University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA.
Zhang W
El-Naggar A K
Lippman S M
Lin P
Lotan R
Xu X C
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