Gene expression of gonadotropin-releasing hormone and its receptor in rat pancreatic cancer cell lines

The regression of experimental and clinical pancreatic cancers by treatment with gonadotropin-releasing hormone (GnRH) agonists or antagonists has been repeatedly reported and is usually presumed to result from the creation of a sex steroid deficiency. There are, however, indications that GnRH analogs can also suppress the growth of the tumor cells in vitro and that specific binding sites for GnRH are present on membranes of these cells. The regulatory role of GnRH in rat pancreatic adenocarcinoma was investigated by examining the gene for GnRH and GnRH receptor (GnRH-R) in two pancreatic tumor cell lines (AR42) and ARIP). Reverse transcriptase polymerase chain reaction and Southern blot analysis indicated both GnRH-mRNA and GnRH-R-mRNA transcripts in the two cell lines. This is the first report raising the possibility of an autocrine/paracrine role for GnRH in rodent malignant pancreas.