The genes for gonadotropin‐releasing hormone and its receptor are expressed in human breast with fibrocystic disease and cancer

While gonadotropin‐releasing hormone (GnRH) or GnRH receptor (GnRHR) have been reported to exist in tissues other than brain and pituitary, there is no report concerning co‐expression of GnRH and GnRHR in human breast tissues. To address this question, we have examined whether mRNA for GnRH as well...

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Veröffentlicht in:International journal of cancer 1997-05, Vol.71 (4), p.595-599
Hauptverfasser: Kottler, Marie‐Laure, Starzec, Anna, Carre, Marie‐Claude, Lagarde, Jean‐Pierre, Martin, Antoine, Counis, Raymond
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Sprache:eng
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Zusammenfassung:While gonadotropin‐releasing hormone (GnRH) or GnRH receptor (GnRHR) have been reported to exist in tissues other than brain and pituitary, there is no report concerning co‐expression of GnRH and GnRHR in human breast tissues. To address this question, we have examined whether mRNA for GnRH as well as GnRHR was present in different human breast samples, by employing the reverse transcription‐polymerase chain reaction (RT‐PCR) protocol followed by Southern blotting of the PCR products. Coexpression of GnRH and GnRHR genes was further confirmed by dot blot hybridization using appropriate [32P]‐labeled probes. We thus tested fibrocystic breast (4 cases), invasive ductal carcinomas (6 cases) and 1 adjacent non‐neoplastic tissue. GnRHR and GnRH mRNAs were found in all actin‐positive samples including malignant as well as nonmalignant tissues. Quantitative determinations of mRNA did not reveal significant differences between malignant and non‐malignant breast samples for either GnRH or GnRHR gene expression. Our data show that neither gene was overexpressed in the breast cancer samples compared with normal breast tissue. Since GnRH agonists inhibit breast epithelial cell growth, the presence of GnRHR mRNA suggests that GnRH may specifically affect breast cell growth. Our data thus raise the possibility of an autocrine/paracrine role for GnRH in human mammary gland. Int. J. Cancer 71:595‐599, 1997. © 1997 Wiley‐Liss, Inc.
ISSN:0020-7136
1097-0215
DOI:10.1002/(SICI)1097-0215(19970516)71:4<595::AID-IJC14>3.0.CO;2-B