Breast Cancer: Basic and Clinical Research

Indira Poola¹, Jessy Abraham¹, Aiyi Liu³, Josephine J. Marshalleck² and Robert L. DeWitty¹

¹Department of Surgery and Breast Center and ²Pathology, Howard University School of Medicine, Washington, DC 20059, and ³Biometry and Mathematical Statistics Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.

Abstract

Background: GPR30 is a cell surface estrogen receptor that has been shown to mediate a number of non-genomic rapid effects of estrogen and appear to balance the signaling of estrogen and growth factors. In addition, progestins appear to use GPR30 for their actions. Therefore, GPR30 could play a critical role in hormonal regulation of breast epithelial cell integrity. Deregulation of the events mediated by GPR30 could contribute to tumorigenesis.

Methods: To understand the role of GPR30 in the deregulation of estrogen signaling processes during breast carcinogenesis, we have undertaken this study to investigate its expression at mRNA levels in tumor tissues and their matched normal tissues. We compared its expression at mRNA levels by RT quantitative real-time PCR relative to GAPDH in ERα”—positive (n = 54) and ERα”—negative (n = 45) breast cancer tissues to their matched normal tissues.

Results: We report here, for the first time, that GPR30 mRNA levels were significantly down-regulated in cancer tissues in comparison with their matched normal tissues (p 0.0001 by two sided paired t-test). The GPR30 expression levels were significantly lower in tumor tissues from patients (n = 29) who had lymph node metastasis in comparison with tumors from patients (n = 53) who were negative for lymph node metastasis (two sample t-test, p 0.02), but no association was found with ERα, PR and other tumor characteristics.

Conclusions: Down-regulation of GPR30 could contribute to breast tumorigenesis and lymph node metastasis.

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