Evidence map›Paper›PMID 24548862›Full record

ArticleBritish journal of cancer2014

Nicotine increases the resistance of lung cancer cells to cisplatin through enhancing Bcl-2 stability.

T Nishioka, L-Y Luo, L Shen, H He, A Mariyannis, W Dai, C Chen

Abstract read
In one paragraph

Article in British journal of cancer, 2014. 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
–field-weighted citation impact
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.

  1. Review
  2. Article
  3. Review
  4. Nicotinic receptors in airway disease.American journal of physiology. Lung cellular and molecular physiology · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Role of the parasympathetic nervous system in cancer initiation and progression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Observational
  16. Review
  17. Review
  18. Article
  19. Article
  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

7 authors.

T NishiokaCenter for Drug Discovery, Northeastern University, 360 Huntington Avenue, Boston, MA 02115, USA.
L-Y LuoThe First Affiliated Hospital of Nanchang University, Nanchang, China.
L ShenCenter for Drug Discovery, Northeastern University, 360 Huntington Avenue, Boston, MA 02115, USA.
H HeThe First Affiliated Hospital of Nanchang University, Nanchang, China.
A MariyannisCenter for Drug Discovery, Northeastern University, 360 Huntington Avenue, Boston, MA 02115, USA.
W DaiDepartments of Environmental Medicine and Biochemistry and Molecular Pharmacology, New York University, Tuxedo, NY, USA.
C Chen1] Center for Drug Discovery, Northeastern University, 360 Huntington Avenue, Boston, MA 02115, USA [2] Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden.

Funding

Study of Ras-Mediated ApoptosisR01CA100498 · NCI · NORTHEASTERN UNIVERSITY · PI CHEN, CHANGYAN · 2004 to 2017
$2.5M
Role of Nicotine in Lung CarcinogenesisR01CA124490 · NCI · NORTHEASTERN UNIVERSITY · PI CHEN, CHANGYAN · 2007 to 2011
$1.6M
NCI NIH HHS R01 CA100498NCI NIH HHS R01 CA124490
6 · The paper itself

Abstract

backgroundNicotine is able to activate mitogenic signalling pathways, which promote cell growth or survival as well as increase chemoresistance of cancer cells. However, the underlying mechanisms are not fully understood.

methodsIn this study, we used immunoblotting and immunoprecipitation methods to test the ubiquitination and degradation of Bcl-2 affected by nicotine in lung cancer cells. Apoptotic assay was also used to measure the antagonising effect of nicotine on cisplatin-mediated cytotoxicity.

resultsWe demonstrated that the addition of nicotine greatly attenuated Bcl-2 ubiquitination and degradation, which further desensitised lung cancer cells to cisplatin-induced cytotoxicity. In this process, Bcl-2 was persistently phosphorylated in the cells cotreated with nicotine and cisplatin. Furthermore, Akt was proven to be responsible for sustained activation of Bcl-2 by nicotine, which further antagonised cisplatin-mediated apoptotic signalling.

conclusionsOur study suggested that nicotine activates its downstream signalling to interfere with the ubiquitination process and prevent Bcl-2 from being degraded in lung cancer cells, resulting in the increase of chemoresistance.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCisplatinDrug Resistance, NeoplasmHumansLung NeoplasmsMiceNicotineProtein Processing, Post-TranslationalProtein StabilityProto-Oncogene Proteins c-bcl-2Tumor Cells, CulturedUbiquitinationUp-RegulationAntineoplastic AgentsCisplatinNicotineProto-Oncogene Proteins c-bcl-2

Identifiers

PMID24548862
PMCPMC3974091

What OpenQuestion holds

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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.