ArticleBMC cancer2004
A novel approach in the treatment of neuroendocrine gastrointestinal tumors: additive antiproliferative effects of interferon-gamma and meta-iodobenzylguanidine.
Article in BMC cancer, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 30 citations in OpenAlex.
- Potential Roles of Enterochromaffin Cells in Early Life Stress-Induced Irritable Bowel Syndrome.Frontiers in cellular neuroscience · 2022Review
- Identification of BST2 Contributing to the Development of Glioblastoma Based on Bioinformatics Analysis.Frontiers in genetics · 2022Article
- Norepinephrine transporter promotes the invasion of human colon cancer cells.Oncology letters · 2020Article
- Nothing but NET: a review of norepinephrine transporter expression and efficacy of 131I-mIBG therapy.Pediatric blood & cancer · 2015Review
- Histone deacetylase inhibitor MS-275 alone or combined with bortezomib or sorafenib exhibits strong antiproliferative action in human cholangiocarcinoma cells.World journal of gastroenterology · 2007Article
- Article
- Signaling pathways involved in the inhibition of epidermal growth factor receptor by erlotinib in hepatocellular cancer.World journal of gastroenterology · 2006Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTherapeutic options to effectively inhibit growth and spread of neuroendocrine gastrointestinal tumors are still limited. As both meta-iodobenzylguanidine (MIBG) and interferon-gamma (IFNgamma) cause antineoplastic effects in neuroendocrine gastrointestinal tumor cells, we investigated the antiproliferative effects of the combination of IFNgamma and non-radiolabeled MIBG in neuroendocrine gut STC-1 and pancreatic carcinoid BON tumor cells. METHODS AND
resultsIFNgamma receptors were expressed in both models. IFNgamma dose- and time-dependently inhibited the growth of both STC-1 and of BON tumor cells with IC50-values of 95 +/- 15 U/ml and 135 +/- 10 U/ml, respectively. Above 10 U/ml IFNgamma induced apoptosis-specific caspase-3 activity in a time-dependent manner in either cell line and caused a dose-dependent arrest in the S-phase of the cell cycle. Furthermore, IFNgamma induced cytotoxic effects in NE tumor cells. The NE tumor-targeted drug MIBG is selectively taken up via norepinephrine transporters, thereby specifically inhibiting growth in NE tumor cells. Intriguingly, IFNgamma treatment induced an upregulation of norepinephrine transporter expression in neuroendocrine tumors cells, as determined by semi-quantitative RT-PCR. Co-application of sub-IC50 concentrations of IFNgamma and MIBG led to additive growth inhibitory effects, which were mainly due to increased cytotoxicity and S-phase arrest of the cell cycle.
conclusionOur data show that IFNgamma exerts antiproliferative effects on neuroendocrine gastrointestinal tumor cells by inducing cell cycle arrest, apoptosis and cytotoxicity. The combination of IFNgamma with the NE tumor-targeted agent MIBG leads to effective growth control at reduced doses of either drug. Thus, the administration of IFNgamma alone and more so, in combination with MIBG, is a promising novel approach in the treatment of neuroendocrine gastrointestinal tumors.
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