Evidence map›Paper›PMID 18844224›Full record

ArticleInternational journal of cancer2009

Nicotine induces cell proliferation, invasion and epithelial-mesenchymal transition in a variety of human cancer cell lines.

Piyali Dasgupta, Wasia Rizwani, Smitha Pillai, Rebecca Kinkade, Michelle Kovacs, Shipra Rastogi, Sarmistha Banerjee, Melanie Carless, Esther Kim, Domenico Coppola and 2 more

Open access · greenAbstract read
In one paragraph

Article in International journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 208 papers.

0numbers the graph read from it
0cells of the map it votes in
208citing papers in PubMed
9.2field-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

208 citing papers in PubMed, 372 citations in OpenAlex.

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148 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

12 authors at 2 institutions in 1 country.

Piyali DasguptaDrug Discovery Program, H Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.
Wasia Rizwani
Smitha Pillai
Rebecca Kinkade
Michelle Kovacs
Shipra Rastogi
Sarmistha Banerjee
Melanie Carless
Esther Kim
Domenico Coppola
Eric Haura
Srikumar Chellappan
University of South Florida · USMoffitt 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
NCI NIH HHS R01 CA127725
6 · The paper itself

Abstract

Cigarette smoking is strongly correlated with the onset of nonsmall cell lung cancer (NSCLC). Nicotine, an active component of cigarettes, has been found to induce proliferation of lung cancer cell lines. In addition, nicotine can induce angiogenesis and confer resistance to apoptosis. All these events are mediated through the nicotinic acetylcholine receptors (nAChRs) on lung cancer cells. In this study, we demonstrate that nicotine can promote anchorage-independent growth in NSCLCs. In addition, nicotine also induces morphological changes characteristic of a migratory, invasive phenotype in NSCLCs on collagen gel. These morphological changes were similar to those induced by the promigratory growth factor VEGF. The proinvasive effects of nicotine were mediated by alpha7-nAChRs on NSCLCs. RT-PCR analysis showed that the alpha7-nAChRs were also expressed on human breast cancer and pancreatic cancer cell lines. Nicotine was found to promote proliferation and invasion in human breast cancer. The proinvasive effects of nicotine were mediated via a nAChR, Src and calcium-dependent signaling pathway in breast cancer cells. In a similar fashion, nicotine could also induce proliferation and invasion of Aspc1 pancreatic cancer cells. Most importantly, nicotine could induce changes in gene expression consistent with epithelial to mesenchymal transition (EMT), characterized by reduction of epithelial markers like E-cadherin expression, ZO-1 staining and concomitant increase in levels of mesenchymal proteins like vimentin and fibronectin in human breast and lung cancer cells. Therefore, it is probable that the ability of nicotine to induce invasion and EMT may contribute to the progression of breast and lung cancers.

Indexed as

CadherinsCell Line, TumorCell ProliferationEpitheliumFibronectinsHumansMesodermModels, BiologicalNeoplasm InvasivenessNicotineNicotinic AgonistsReceptors, NicotinicSmokingVimentinWound HealingCadherinsFibronectinsNicotineNicotinic AgonistsReceptors, NicotinicVimentin

Identifiers

PMID18844224
PMCPMC2826200
OpenAlexW2056548559

What OpenQuestion holds

Textmetadata
LicenceTDM
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.