Reduced NGF secretion by HT-29 human colon cancer cells treated with a GRPR antagonist.

The gastrin-releasing peptide receptor (GRPR) is a therapeutic target in colon cancer. Here we show that the GRPR antagonist RC-3095 (10(-3), 10(-6), or 1 microM) decreases nerve growth factor (NGF) secretion measured by enzyme-linked immunosorbent assay (ELISA) in HT-29 human colon carcinoma cells. The results suggest that decreased secretion of neurotrophins might be a novel mechanism by which GRPR antagonists exert their antiproliferative effects in cancer cells.

Stimulation of proliferation of U138-MG glioblastoma cells by gastrin-releasing peptide in combination with agents that enhance cAMP signaling.

Increasing evidence indicates that gastrin-releasing peptide (GRP) acts as an autocrine growth factor for brain tumors. However, it remains unclear whether the cAMP/protein kinase A (PKA) signaling pathway plays a role in mediating the mitogenic effects of GRP. We show here that GRP combined with agents that stimulate the cAMP/PKA pathway promotes proliferation of human gliobastoma cells.

Gastrin-releasing peptide receptors regulate proliferation of C6 Glioma cells through a phosphatidylinositol 3-kinase-dependent mechanism.

Gastrin-releasing peptide (GRP) has been proposed as a major growth factor in brain tumors, and GRP receptor (GRPR) antagonists show antiproliferative effects in experimental gliomas. However, the underlying molecular events downstream of GRPR activation remain poorly understood. In the present study, we examined the role of the GRPR in regulating proliferation of glioma cells in vitro and its possible interaction with the phosphatidylinositol 3-kinase (PI3K) signaling pathway.

Cross-reactive IgE antibody responses to tropomyosins from Ascaris lumbricoides and cockroach.

Background: Evidence indicates that infection with Ascaris lumbricoides may promote development of allergy and asthma.

Objective: To study the role of tropomyosin, a pan-allergen in invertebrates, in IgE responses to A lumbricoides.

Methods: Recombinant A lumbricoides and Periplaneta americana tropomyosins were expressed in Pichia pastoris.

Angiotensin II potentiates inflammatory edema in rats: Role of mast cell degranulation.

The aim of this study was to evaluate the effect of angiotensin II on models of acute inflammation. This study shows that angiotensin II potentiates the carrageenan- and dextran-induced paw edema. The administration of angiotensin II does not change the myeloperoxidase activity, neither the tissue content of interleukin-1 beta and tumor necrosis alpha nor the neutrophil migration to the peritoneal cavity, but induces significant enhancement of mast cell degranulation.