Evidence map›Paper›PMID 20727180›Full record

ArticleMolecular cancer2010

Nicotine-induced survival signaling in lung cancer cells is dependent on their p53 status while its down-regulation by curcumin is independent.

Vineshkumar T Puliyappadamba, Vino T Cheriyan, Arun Kumar T Thulasidasan, Smitha V Bava, Balachandran S Vinod, Priya R Prabhu, Ranji Varghese, Arathy Bevin, Shalini Venugopal, Ruby John Anto

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

25 citing papers in PubMed, 57 citations in OpenAlex.

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  14. Nicotine Prevents and Reverses Paclitaxel-Induced Mechanical Allodynia in a Mouse Model of CIPN.The Journal of pharmacology and experimental therapeutics · 2018
    Article
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  19. Connections of nicotine to cancer.Nature reviews. Cancer · 2014
    Review
  20. Article
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

10 authors at 1 institution in 1 country.

Vineshkumar T PuliyappadambaIntegrated Cancer Research Program, Division of Cancer Research, Rajiv Gandhi Centre for Biotechnology, Thiruvananthapuram, Kerala, India.
Vino T Cheriyan
Arun Kumar T Thulasidasan
Smitha V Bava
Balachandran S Vinod
Priya R Prabhu
Ranji Varghese
Arathy Bevin
Shalini Venugopal
Ruby John Anto
Rajiv Gandhi Centre for Biotechnology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung cancer is the most lethal cancer and almost 90% of lung cancer is due to cigarette smoking. Even though nicotine, one of the major ingredients of cigarette smoke and the causative agent for addiction, is not a carcinogen by itself, several investigators have shown that nicotine can induce cell proliferation and angiogenesis. We observed that the proliferative index of nicotine is different in the lung cancer cell lines H1299 (p53-/-) and A549 (p53+/+) which indicates that the mode of up-regulation of survival signals by nicotine might be different in cells with and without p53.

resultsWhile low concentrations of nicotine induced activation of NF-κB, Akt, Bcl2, MAPKs, AP1 and IAPs in H1299, it failed to induce NF-κB in A549, and compared to H1299, almost 100 times higher concentration of nicotine was required to induce all other survival signals in A549. Transfection of WT-p53 and DN-p53 in H1299 and A549 respectively, reversed the mode of activation of survival signals. Curcumin down-regulated all the survival signals induced by nicotine in both the cells, irrespective of their p53 status. The hypothesis was confirmed when lower concentrations of nicotine induced NF-κB in two more lung cancer cells, Hop-92 and NCI-H522 with mutant p53 status. Silencing of p53 in A549 using siRNA made the cells susceptible to nicotine-induced NF-κB nuclear translocation as in A549 DN-p53 cells.

conclusionsThe present study reveals a detrimental role of nicotine especially in lung cancer patients with impaired p53 status and identifies curcumin as a potential chemopreventive.

Indexed as

Cell Line, TumorCell ProliferationCurcuminCyclin D1Cyclooxygenase 2Down-RegulationHumansLung NeoplasmsNicotinePhosphorylationProto-Oncogene Proteins c-aktSignal TransductionTranscription Factor AP-1Tumor Suppressor Protein p53CurcuminCyclin D1Cyclooxygenase 2NicotineProto-Oncogene Proteins c-aktTranscription Factor AP-1Tumor Suppressor Protein p53

Identifiers

PMID20727180
PMCPMC2936340
OpenAlexW2171990116

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Registered trials

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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.