학술논문

Expression of estrogen receptor [beta] wt isoform (ER[beta]1) and ER[beta]I5 splice variant mRNAs in sporadic breast cancer
Document Type
Author abstract
Source
Journal of Cancer Research and Clinical Oncology. August, 2007, Vol. 133 Issue 8, p571, 9 p.
Subject
Postmenopausal women -- Physiological aspects
Breast cancer -- Physiological aspects
Estrogen -- Physiological aspects
Language
English
ISSN
0171-5216
Abstract
Purpose In addition to Estrogen Receptor [alpha] (ER[alpha]) and Progesterone Receptor (PR), the Second Estrogen Receptor (ER[beta]) appears to play an important role not only in estrogen signaling, but also in the pathogenesis of cancer in estrogen dependent tissues. The existence of various isoforms and splice variants of both ERs additionally complicates elucidation of their physiological role and involvement in the process of carcinogenesis. Methods In this study, the expression of ER[beta]1 mRNA (wild type of [beta] receptor) and splice variant ER[beta]I5 mRNA (which codes for truncated protein) was measured by the quantitative RT-PCR (q RT-PCR) in the 60 samples of Breast Cancer (BC) and correlated with ER[alpha] and PR protein levels and with clinical and histopathological parameters. Results We found the inverse correlation of ER[beta]I5 mRNA expression with the levels of PR and ER[alpha] proteins in the group of postmenopausal patients we also report the lower expression of ER[beta]1 and ER[beta]I5 mRNA in the larger tumors (> 20 mm, T2, and T3) than in smaller ones (a$?20 mm, T1). The decrease of ER[beta]I5 mRNA expression in larger tumors is found to arise from ER-positive breast carcinomas. In addition, the portion of tumors with concomitant high expression of both transcripts matches up the known percentage of tumors resistant to endocrine therapy in patients with different ER/PR status. Conclusions As far as we know, this is the first study in which ER[beta]I5 mRNA splice variant was quantified by real-time RT-PCR in the clinical samples of breast cancer tissue. Until now, the focus of clinical reports was the level of ER[beta]1, ER[beta]2, and ER[beta]5 isoforms. The higher expression of ER[beta]I5 mRNA is associated with the indicators of low biological aggressiveness of tumor (low tumor size within ER-positive status in our study) suggesting that the uncontrolled local tumor growth may occur as the expression of ER[beta]I5 mRNA decreases in estrogen-dependent breast cancer.