Nicotine, acetylcholine and bombesin are trophic growth factors in neuroendocrine cell lines derived from experimental hamster lung tumors
Abstract
Neuroendocrine hamster lung tumors, induced by exposure to 60% hyperoxia and subcutaneous administration of the tobacco-specific nitrosamine 4-(methylnitrosamino)-l-(3-pyridyl)-l-butanone (NNK) for 12 weeks, were placed in cell culture. By subsequent selective transfer of epithelial cells and maintenance in an atmosphere of 8% CO2, cell lines with characteristics of neuroendocrine cells were established. The neuroendocrine markers expressed by these cell lines included electron dense neuroendocrine secretion granules as well as secretion of calcitonin and mammalian bombesin. In keeping with data previously reported for a human neuroendocrine lung tumor cell line, nicotine, acetylcholine, and mammalian bombesin (MB) acted as strong growth factors in these neuroendocrine hamster tumor lines. The mitogenic effect of nicotine and acetylcholine was abolished by nicotinic receptor inhibition while the effects of mammalian bombesin were inhibited by an antagonist of MB receptors. Our data suggest that a receptor-mediated mitogenic effect of nicotine on neuroendocrine lung cells may be instrumental in the induction of smoking-associated small cell lung cancer.
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Different groups observed that respiration hyperoxia can act as a promoting stimulus to induce lung tumorigenesis of neuroendocrine tumors.
“Conversely, different groups have observed that respiration hyperoxia can act as a promoting stimulus to induce lung tumorigenesis of neuroendocrine tumors.”
From Hypoxia signaling in cancer: Implications for therapeutic interventions (2023) · cites this paper as [289]
Respiratory hyperoxia in the early stages of tumorigenesis accelerates tumor development by promoting angiogenesis.
“respiratory hyperoxia in the early stages of tumorigenesis accelerates tumor development by promoting angiogenesis.”
From Hypoxia signaling in cancer: Implications for therapeutic interventions (2023) · cites this paper as [289]
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- Authors
- Schüller, H. M., Nylen, E., Park, P., & Becker, K. L.
- Affiliations
- George Washington University (US)
- ORCID
- Nylen, Eric
- Venue
- Life Sciences
- Publisher
- Elsevier BV
- Published
- 1990-01
- Volume
- 47
- Issue
- 6
- Pages
- 571-578
- ISSN
- 0024-3205 (ISSN-L)
- OpenAlex
- W2058610321
- Cited by
- 36
- References
- 20
- Citations by year
- 2023: 1 · 2020: 1 · 2019: 1 · 2017: 1 · 2016: 2 · 2015: 1 · 2013: 1 · 2012: 1
- FWCI
- 2.61
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Life Sciences (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ca048014-06)
- National Cancer Institute (R01 CA48014-02)
- Topics
- Health Sciences › Medicine › Epidemiology › Neuroendocrine Tumor Research Advances
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Health Sciences › Medicine › Oncology › Lung Cancer Research Studies
- Keywords
- nicotine, acetylcholine, bombesin, lung neuroendocrine tumors, small cell lung cancer, cancer cell lines, mitogenic growth factors, nicotinic acetylcholine receptors, bombesin receptor, hyperoxia, NNK, tobacco smoke, hamster
- MeSH terms
- Acetylcholine, Adrenergic beta-Agonists, Adrenergic beta-Antagonists, Animals, Bombesin, Cell Division, Growth Substances, Cricetinae, Male, Mesocricetus, Nicotine, Receptors, Nicotinic, Substance P, Tumor Cells, Cultured, Receptors, Neurotransmitter, Receptors, Bombesin, Nicotinic Antagonists
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