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Related Concept Videos

Drugs Acting on Autonomic Ganglia: Stimulants01:23

Drugs Acting on Autonomic Ganglia: Stimulants


Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...
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Related Experiment Video

Updated: Jul 13, 2026

Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition
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Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition

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Nicotine, lung and cancer.

Alessia Grozio1, Alessia Catassi, Zita Cavalieri

  • 1Translational Research B (Lung Cancer), Department of Integrated Medical Oncology (DOMI), National Cancer Institute, Largo Rosanna Benzi 10, Genoa, Italy. alessia.grozio@libero.it

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Nicotine exposure may promote tumor growth and survival by activating proliferative pathways and preventing apoptosis, but does not initiate cancer itself. This impacts understanding of lung cancer progression and treatment strategies.

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Area of Science:

  • Oncology
  • Cell Biology
  • Pharmacology

Background:

  • The respiratory epithelium expresses nicotinic acetylcholine receptors (nAChRs), with distinct repertoires in bronchial epithelial cells (BEC) and small airway epithelial cells (SAEC).
  • nAChRs on lung carcinoma and mesothelioma cells contribute to an autocrine-proliferative network, driving neoplastic cell growth.
  • Nicotine and tobacco carcinogens like NNK and NNN are implicated in promoting the proliferation of various cancer cell lines and endothelial cells.

Purpose of the Study:

  • To investigate the role of nicotine and nAChRs in cancer proliferation and progression.
  • To elucidate the mechanisms by which nicotine influences tumor growth, including growth factor secretion and signaling pathways.
  • To determine if nicotine itself can initiate cancer or merely promote the growth of existing tumors.

Main Methods:

  • Analysis of nAChR expression in normal and cancerous lung epithelial cells (BEC and SAEC).
  • In vitro studies on the effects of nicotine and carcinogens on cancer cell line proliferation.
  • In vivo studies assessing nicotine's impact on solid tumor growth.
  • Examination of nicotine-induced changes in growth factor secretion, protein expression (calpain, COX-2, VEGFR-2), and signaling pathway activation (Raf/MEK/ERK).
  • Assessment of nicotine's effect on apoptosis induced by chemotherapeutic agents in non-small cell lung cancer (NSCLC).

Main Results:

  • Nicotine promotes the growth of various cancer cells and endothelial cells, potentially through autocrine-proliferative networks involving nAChRs.
  • Nicotine induces secretion of growth factors (bFGF, TGF-alpha, VEGF, PDGF) and upregulates proteins like COX-2 and VEGFR-2, activating the Raf/MEK/ERK pathway.
  • Nicotine has been shown to promote solid tumor growth in vivo, suggesting a role in tumor progression rather than initiation.
  • Nicotine can prevent apoptosis induced by various agents, including chemotherapy in NSCLC, conferring a survival advantage to cancer cells.

Conclusions:

  • While tobacco carcinogens initiate and promote tumorigenesis, nicotine exposure appears to confer a proliferative and survival advantage to early-stage tumors.
  • Nicotine's pro-proliferative and anti-apoptotic effects contribute to cancer progression and treatment resistance.
  • There is no evidence that nicotine itself provokes cancer, but its role in promoting growth and survival of existing tumors is significant.