Evidence map›Paper›PMID 19911375›Full record

ArticleJournal of cellular biochemistry2010

Nicotine, through upregulating pro-survival signaling, cooperates with NNK to promote transformation.

Takashi Nishioka, Jinjin Guo, Daisuke Yamamoto, Lihua Chen, Petra Huppi, Chang Yan Chen

Abstract read
In one paragraph

Article in Journal of cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Ambient fine particulate matter inhibits 15-lipoxygenases to promote lung carcinogenesis.Journal of experimental & clinical cancer research : CR · 2019
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Connections of nicotine to cancer.Nature reviews. Cancer · 2014
    Review
  11. Article
  12. Review
  13. Nicotine and lung cancer.Journal of carcinogenesis · 2013
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. [Current status of Akt in non-small cell lung cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2010
    Review
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

6 authors at 2 institutions in 2 countries.

Takashi NishiokaDepartment of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Jinjin Guo
Daisuke Yamamoto
Lihua Chen
Petra Huppi
Chang Yan Chen
Beth Israel Deaconess Medical Center · USUniversity of Geneva · CH

Funding

Role of Nicotine in Lung CarcinogenesisR01CA124490 · NCI · NORTHEASTERN UNIVERSITY · PI CHEN, CHANGYAN · 2007 to 2011
$1.6M
NCI NIH HHS R01 CA124490
6 · The paper itself

Abstract

Cigarette smoking is a mixture of thousands of compounds, many of which are carcinogens, such as NNK [4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone]. Nicotine, as an addictive substance in cigarette, has been shown to promote growth of non-neuronal cells. It is unclear how nicotine cooperates with tobacco-related carcinogens during tumorigenesis. Here, by concurrent treatment of nicotine and NNK, we investigate the effect of the cooperation of these two compounds on cell growth and apoptosis in various different lung epithelial (RLE) or cancer (LKR) cells. We demonstrated that short-term nicotine exposure moderately activated mitogenic signaling pathways (such as PKC, ERK, and Akt) and a mediocre protection against cisplatin-mediated apoptosis. In contrast, NNK strongly stimulated mitogenic signaling and rendered the cells a high resistance to cisplatin. The pre-ligation of nAChR by nicotine interfered with NNK-mediated mitogenic signaling and resistance to cisplatin, the magnitude of which was similar as that exposed to nicotine alone. Interestingly, a week after the exposure to nicotine or nicotine plus NNK, Bcl-2 expression was augmented, accompanied with the increased resistance to cisplatin-induced apoptosis. In comparison, long-term NNK treatment provided very little protection of the cells from cisplatin. We also showed that the combination treatment promoted more cells to grow in an anchorage-independent fashion than NNK exposure alone. Thus, the data suggest that through occupying nAChR, nicotine appears to modulate NNK-mediated signaling and persistently sustain pro-survival activities to promote transformation.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCarcinogensCell ProliferationCell Transformation, NeoplasticCisplatinDNA FragmentationHumansImmunoblottingMiceNicotineNicotinic AgonistsNitrosaminesRatsReceptors, Nicotinic4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanoneAntineoplastic AgentsCarcinogensCisplatinNicotineNicotinic AgonistsNitrosaminesReceptors, Nicotinic

Identifiers

PMID19911375
PMCPMC3683296
OpenAlexW2085086439

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.