Evidence map›Paper›PMID 26909550›Full record

ArticlePloS one2016

Nicotine Inhibits Cisplatin-Induced Apoptosis via Regulating α5-nAChR/AKT Signaling in Human Gastric Cancer Cells.

Yanfei Jia, Haiji Sun, Hongqiao Wu, Huilin Zhang, Xiuping Zhang, Dongjie Xiao, Xiaoli Ma, Yunshan Wang

Abstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Cholinergic Mechanisms in Gastrointestinal Neoplasia.International journal of molecular sciences · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. 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
  15. Article
  16. Article
  17. Article
  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

8 authors.

Yanfei JiaCentral Laboratory, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Haiji SunCollege of Life Science, Shandong Normal University, Jinan, China.
Hongqiao WuCentral Laboratory, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Huilin ZhangCentral Laboratory, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Xiuping ZhangCentral Laboratory, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Dongjie XiaoCentral Laboratory, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Xiaoli MaCentral Laboratory, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Yunshan WangCentral Laboratory, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer incidence demonstrates a strong etiologic association with smoking. Nicotine, the major component in tobacco, is a survival agonist that inhibits apoptosis induced by certain chemotherapeutic agents, but the precise mechanisms involved remain largely unknown. Recently studies have indicated that α5-nicotinic acetylcholine receptor (α5-nAChR) is highly associated with lung cancer risk and nicotine dependence. Nevertheless, no information has been available about whether nicotine also affects proliferation of human gastric cancer cells through regulation of α5-nAChR. To evaluate the hypothesis that α5-nAChR may play a role in gastric cancer, we investigated its expression in gastric cancer tissues and cell lines. The expression of α5-nAChR increased in gastric cancer tissue compared with para-carcinoma tissues. In view of the results, we proceeded to investigate whether nicotine inhibits cisplatin-induced apoptosis via regulating α5-nAChR in gastric cancer cell. The results showed that nicotine significantly promoted cell proliferation in a dose and time-dependent manner through α5-nAChR activation in human gastric cells. Furthermore, nicotine inhibited apoptosis induced by cisplatin. Silence of α5-nAChR ablated the protective effects of nicotine. However, when co-administrating LY294002, an inhibitor of PI3K/AKT pathway, an increased apoptosis was observed. This effect correlated with the induction of Bcl-2, Bax, Survivin and Caspase-3 by nicotine in gastric cell lines. These results suggest that exposure to nicotine might negatively impact the apoptotic potential of chemotherapeutic drugs and that α5-nAChR/AKT signaling plays a key role in the anti-apoptotic activity of nicotine induced by cisplatin.

Indexed as

CisplatinNicotineStomach NeoplasmsApoptosisCell Line, TumorFemaleHumansMaleProto-Oncogene Proteins c-aktReceptors, NicotinicSignal TransductionCisplatinNicotineProto-Oncogene Proteins c-aktReceptors, Nicotinic

Identifiers

PMID26909550
PMCPMC4765889

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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.