Evidence map›Paper›PMID 24398389›Full record

ReviewMolecular cancer research : MCR2014

Nicotine-mediated cell proliferation and tumor progression in smoking-related cancers.

Courtney Schaal, Srikumar P Chellappan

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular cancer research : MCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
188citing papers in PubMed, 3 pooled it
13.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

188 citing papers in PubMed, 3 syntheses or guidelines pooled it, 332 citations in OpenAlex.

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  18. Journal of pharmacy & bioallied sciences · 2025
    Article
  19. Effect of smoking on the recurrence and progression of non-muscle-invasive bladder cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  20. Article

128 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Courtney SchaalDepartment of Tumor Biology, H. Lee Moffitt Cancer Center and Research Institute, 12902 Magnolia Drive, Tampa, FL 33612. Srikumar.Chellappan@moffitt.org.
Srikumar P Chellappan
Moffitt Cancer Center · US

Funding

Role of Beta-arrestin-1 and Src in nAChR Signaling and Lung CaancerR01CA127725 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI CHELLAPPAN, SRIKUMAR P. · 2008 to 2012
$1.7M
Role of Id1 in NSCLC Progression and MetastasisR01CA139612 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI CHELLAPPAN, SRIKUMAR P. · 2009 to 2013
$1.4M
NCI NIH HHS CA127725NCI NIH HHS CA139612NCI NIH HHS R01 CA127725NCI NIH HHS R01 CA139612
6 · The paper itself

Abstract

Tobacco smoke contains multiple classes of established carcinogens including benzo(a)pyrenes, polycyclic aromatic hydrocarbons, and tobacco-specific nitrosamines. Most of these compounds exert their genotoxic effects by forming DNA adducts and generation of reactive oxygen species, causing mutations in vital genes such as K-Ras and p53. In addition, tobacco-specific nitrosamines can activate nicotinic acetylcholine receptors (nAChR) and to a certain extent β-adrenergic receptors (β-AR), promoting cell proliferation. Furthermore, it has been demonstrated that nicotine, the major addictive component of tobacco smoke, can induce cell-cycle progression, angiogenesis, and metastasis of lung and pancreatic cancers. These effects occur mainly through the α7-nAChRs, with possible contribution from the β-ARs and/or epidermal growth factor receptors. This review article will discuss the molecular mechanisms by which nicotine and its oncogenic derivatives such as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and N-nitrosonornicotine induce cell-cycle progression and promote tumor growth. A variety of signaling cascades are induced by nicotine through nAChRs, including the mitogen-activated protein kinase/extracellular signal-regulated kinase pathway, phosphoinositide 3-kinase/AKT pathway, and janus-activated kinase/STAT signaling. In addition, studies have shown that nAChR activation induces Src kinase in a β-arrestin-1-dependent manner, leading to the inactivation of Rb protein and resulting in the expression of E2F1-regulated proliferative genes. Such nAChR-mediated signaling events enhance the proliferation of cells and render them resistant to apoptosis induced by various agents. These observations highlight the role of nAChRs in promoting the growth and metastasis of tumors and raise the possibility of targeting them for cancer therapy.

Indexed as

ApoptosisCell CycleCell ProliferationDisease ProgressionDNA DamageE2F1 Transcription FactorHumansLung NeoplasmsMAP Kinase Signaling SystemNeoplasm MetastasisNicotianaNicotineNicotinic AgonistsReceptors, NicotinicRetinoblastoma ProteinSmokingE2F1 protein, humanE2F1 Transcription FactorNicotineNicotinic AgonistsReceptors, NicotinicRetinoblastoma Protein

Identifiers

PMID24398389
PMCPMC3915512
OpenAlexW2120364751

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.