Premium
Cyclooxygenase‐2 mRNA expression correlates with aromatase expression in human breast cancer
Author(s) -
Salhab M.,
SinghRanger G.,
Mokbel R.,
Jouhra F.,
Jiang W.G.,
Mokbel K.
Publication year - 2007
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.20740
Subject(s) - aromatase , breast cancer , estrogen , medicine , cyclooxygenase , messenger rna , gene expression , downregulation and upregulation , endocrinology , cancer , cancer research , enzyme , biology , gene , biochemistry
The cyclooxygenase‐2 (COX‐2), responsible for the conversion of arachidonic acid into prostaglandin (PG) E2, is known to increase intracellular cAMP and estrogen production in malignant breast tissue. The aromatase enzyme complex is responsible for local production of estrogens in breast cancer. Increasing evidence supports a role for COX‐2 in upregulation of aromatase activity. The aim of this study was to examine the relationship between COX‐2 and aromatase mRNA expression in human breast cancer. Methods A total of 160 breast samples (127 tumor tissues and 33 normal tissues) were analyzed. Levels of transcription were determined using real‐time quantitative PCR. COX‐2 and aromatase mRNA expression were normalized against CK19. Levels of expression of COX‐2 were correlated with those of aromatase using Pearson's correlation method. Results Levels of expression of COX‐2/CK19 of both benign and malignant tissues were positively correlated with aromatase/CK19 transcript levels (correlation coefficient = +0.536, P < 0.0001). When we compared levels of expression of both genes in malignant samples only, there was a highly significant positive correlation (r = +0.611, P < 0.00001). Conclusion This study demonstrates a strong positive relationship between COX‐2 and aromatase mRNA expression, and lends further support to the hypothesis that COX‐2 is an upregulator of aromatase in breast tissue. J. Surg. Oncol. 2007;96:424–428. © 2007 Wiley‐Liss, Inc.