Anti-proliferative effect of the gastrin-release peptide receptor antagonist RC-3095 plus temozolomide in experimental glioblastoma models

Oliveira, Marianne Schrader de; Cechim, Giovana; Braganhol, Elisandra; Santos, Daniel Garcia dos; Meurer, Luíse; Castro, Cláudio Galvão de; Brunetto, Algemir Lunardi; Schwartsmann, Gilberto; Battastini, Ana Maria Oliveira; Lenz, Guido; Roesler, Rafaël

doi:10.1007/s11060-009-9851-2

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“…GRP and bombesin have been shown to have mitogenic activity and increase proliferation and growth of a variety of cancers including lung [44], prostate [45,46], breast, gastric [47,48], pancreatic [49], colorectal cancers [50], neuroblastoma [51], and glioma [52,53]. Consistent with these data, our studies demonstrated the stimulation of proliferation of Ace-1-huGRPr cells by bombesin in vitro and increased tumor volume and weight in bombesin-treated mice.…”

Section: Discussionsupporting

confidence: 88%

Gastrin-releasing peptide receptor (GRPr) promotes EMT, growth, and invasion in canine prostate cancer

et al. 2016

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BACKGROUND The gastrin-releasing peptide receptor (GRPr) is upregulated in early and late-stage human prostate cancer (PCa) and other solid tumors of the mammary gland, lung, head and neck, colon, uterus, ovary, and kidney. However, little is known about its role in prostate cancer. This study examined the effects of a heterologous GRPr agonist, bombesin (BBN), on growth, motility, morphology, gene expression, and tumor phenotype of an osteoblastic canine prostate cancer cell line (Ace-1) in vitro and in vivo. METHODS The Ace-1 cells were stably transfected with the human GRPr and tumor cells were grown in vitro and as subcutaneous and intratibial tumors in nude mice. The effect of BBN was measured on cell proliferation, cell migration, tumor growth (using bioluminescence), tumor cell morphology, bone tumor phenotype, and epithelial-mesenchymal transition (EMT) and metastasis gene expression (quantitative RT-PCR). GRPr mRNA expression was measured in primary canine prostate cancers and normal prostate glands. RESULTS Bombesin (BBN) increased tumor cell proliferation and migration in vitro and tumor growth and invasion in vivo. BBN upregulated epithelial-to-mesenchymal transition (EMT) markers (TWIST, SNAIL, and SLUG mRNA) and downregulated epithelial markers (E-cadherin and β-catenin mRNA), and modified tumor cell morphology to a spindle cell phenotype. Blockade of GRPr upregulated E-cadherin and downregulated VIMENTIN and SNAIL mRNA. BBN altered the in vivo tumor phenotype in bone from an osteoblastic to osteolytic phenotype. Primary canine prostate cancers had increased GRPr mRNA expression compared to normal prostates. CONCLUSION These data demonstrated that the GRPr is important in prostate cancer growth and progression and targeting GRPr may be a promising strategy for treatment of prostate cancer.

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