ArticleBiochimica et biophysica acta2013
Gastrointestinal hormones stimulate growth of Foregut Neuroendocrine Tumors by transactivating the EGF receptor.
Article in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- Extracellular signalling regulates gastrin transcription through site-specific phosphorylation and nuclear redistribution of Menin.bioRxiv : the preprint server for biology · 2026Article
- Article
- Review
- Adding of neurotensin to non-small cell lung cancer cells increases tyrosine phosphorylation of HER3.Peptides · 2022Article
- Neurotensin: A novel mediator of ovulation?FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Bombesin Receptor Family Activation and CNS/Neural Tumors: Review of Evidence Supporting Possible Role for Novel Targeted Therapy.Frontiers in endocrinology · 2021Review
- Neuropeptide bombesin receptor activation stimulates growth of lung cancer cells through HER3 with a MAPK-dependent mechanism.Biochimica et biophysica acta. Molecular cell research · 2020Article
- Neurotensin receptors regulate transactivation of the EGFR and HER2 in a reactive oxygen species-dependent manner.European journal of pharmacology · 2019Article
- A possible new target in lung-cancer cells: The orphan receptor, bombesin receptor subtype-3.Peptides · 2018Article
- Neuropeptide G Protein-Coupled Receptors as Oncotargets.Frontiers in endocrinology · 2018Review
- Role of tumor microenvironment in tumorigenesis.Journal of Cancer · 2017Review
- Vasoactive intestinal peptide/pituitary adenylate cyclase activating polypeptide, and their receptors and cancer.Current opinion in endocrinology, diabetes, and obesity · 2016Review
- Review
- Activation of matrix metalloproteinase-9 (MMP-9) by neurotensin promotes cell invasion and migration through ERK pathway in gastric cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Neurotensin, a novel target of Wnt/β-catenin pathway, promotes growth of neuroendocrine tumor cells.International journal of cancer · 2015Article
- Bombesin receptor subtype 3 as a potential target for obesity and diabetes.Expert opinion on therapeutic targets · 2015Review
- Role of Wnt5a in the differentiation of human embryonic stem cells into endometrium-like cells.International journal of clinical and experimental pathology · 2015Article
- PI3K-AKT-mTOR-signaling and beyond: the complex network in gastroenteropancreatic neuroendocrine neoplasms.Theranostics · 2014Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Foregut neuroendocrine tumors [NETs] usually pursuit a benign course, but some show aggressive behavior. The treatment of patients with advanced NETs is marginally effective and new approaches are needed. In other tumors, transactivation of the EGF receptor (EGFR) by growth factors, gastrointestinal (GI) hormones and lipids can stimulate growth, which has led to new treatments. Recent studies show a direct correlation between NET malignancy and EGFR expression, EGFR inhibition decreases basal NET growth and an autocrine growth effect exerted by GI hormones, for some NETs. To determine if GI hormones can stimulate NET growth by inducing transactivation of EGFR, we examined the ability of EGF, TGFα and various GI hormones to stimulate growth of the human foregut carcinoid,BON, the somatostatinoma QGP-1 and the rat islet tumor,Rin-14B-cell lines. The EGFR tyrosine-kinase inhibitor, AG1478 strongly inhibited EGF and the GI hormones stimulated cell growth, both in BON and QGP-1 cells. In all the three neuroendocrine cell lines studied, we found EGF, TGFα and the other growth-stimulating GI hormones increased Tyr(1068) EGFR phosphorylation. In BON cells, both the GI hormones neurotensin and a bombesin analogue caused a time- and dose-dependent increase in EGFR phosphorylation, which was strongly inhibited by AG1478. Moreover, we found this stimulated phosphorylation was dependent on Src kinases, PKCs, matrix metalloproteinase activation and the generation of reactive oxygen species. These results raise the possibility that disruption of this signaling cascade by either EGFR inhibition alone or combined with receptor antagonists may be a novel therapeutic approach for treatment of foregut NETs/PETs.
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