title: LHRH might act as a negative autocrine regulator of proliferation of human ovarian cancer.
abstract: OBJECTIVE
  More than 80% of human ovarian cancers express LHRH and its receptor. The proliferation of human ovarian cancer cell lines is reduced by both LHRH agonists and antagonists. This study was designed to further clarify the possible biological function of this LHRH system.
  
  
  METHODS
  As LHRH agonists and antagonists uniformly reduce proliferation of human ovarian cancer in a dose-dependent way, the effect of low concentrations of authentic LHRH was studied. In addition, longer periods of treatment (up to 9 days) were analyzed. To assess the physiological role of LHRH produced by ovarian cancer cells it was neutralized by adequate concentrations of a specific LHRH antiserum.
  
  
  METHODS
  Human ovarian cancer cells EFO-21 and EFO-27, which express LHRH and its receptor, were incubated for 1-9 days with increasing concentrations (1pmol/l to 10 micromol/l) of authentic LHRH or with concentrations of LHRH antiserum capable of neutralizing at least 1nmol/l LHRH. Proliferation was assessed by counting cells.
  
  
  CONCLUSIONS
  Authentic LHRH reduced time- and dose-dependently proliferation (by maximally mean+/-s.e.m. 32.7 +/- 4.4%, Newman-Keuls, P < 0.001) of both ovarian cancer cell lines. At very low concentrations (1pmol/l) a marginal reduction of proliferation or no effect was observed. A mitogenic effect of authentic LHRH was never detected. Treatment of ovarian cancer cell cultures with antiserum to LHRH significantly increased (up to mean+/-s.e.m. 121.0 +/- 2.8% of controls, Newman-Keuls P <0.001) proliferation of EFO-21 and EFO-27 cells. These findings suggest that LHRH produced by human ovarian cancer cells might act as a negative autocrine regulator of proliferation.
authors.affiliation: Departments of Gynecology and Obstetrics, Georg-August University, Robert-Koch-Street 40, D-37075, Göttingen, Germany.
authors.forename: G
authors.initials: G
authors.lastname: Emons
authors.forename: S
authors.initials: S
authors.lastname: Weiss
authors.forename: O
authors.initials: O
authors.lastname: Ortmann
authors.forename: C
authors.initials: C
authors.lastname: Gründker
authors.forename: K D
authors.initials: KD
authors.lastname: Schulz
mesh_terms: D002288:Adenocarcinoma, Mucinous / Q000473:pathology / Q000503:physiopathology*; D000231:Adenocarcinoma, Papillary / Q000473:pathology / Q000503:physiopathology*; D019898:Autocrine Communication; D002455:Cell Division / Q000187:drug effects / Q000502:physiology; D002460:Cell Line; D018284:Cystadenocarcinoma, Serous / Q000473:pathology / Q000503:physiopathology*; D004305:Dose-Response Relationship, Drug; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000276:immunology / Q000494:pharmacology / Q000502:physiology*; D006801:Humans; D007106:Immune Sera / Q000494:pharmacology; D010051:Ovarian Neoplasms / Q000473:pathology / Q000503:physiopathology*; D013997:Time Factors
chemical_list: D007106:Immune Sera; D007987:Gonadotropin-Releasing Hormone