Evidence map›Paper›PMID 26877709›Full record

ArticleCancer cell international2016

Heat shock protein 27 downstream of P38-PI3K/Akt signaling antagonizes melatonin-induced apoptosis of SGC-7901 gastric cancer cells.

Wenjie Deng, Yujie Zhang, Luo Gu, Jie Cui, Biao Duan, Yueyuan Wang, Jun Du

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. miR-340 Inhibits Proliferation and Induces Apoptosis in Gastric Cancer Cell Line SGC-7901, Possibly via the AKT Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2017
    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 at 1 institution in 1 country.

Wenjie DengCancer Center, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029 China ; Department of Physiology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029 China.
Yujie ZhangCancer Center, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029 China.
Luo GuCancer Center, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029 China ; Department of Physiology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029 China ; Department of Biochemistry and Molecular Biology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029 China.
Jie CuiDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029 China.
Biao DuanDepartment of Physiology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029 China.
Yueyuan WangDepartment of Physiology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029 China.
Jun DuCancer Center, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029 China ; Department of Physiology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029 China.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDespite the fact that melatonin treatment shows some promise in gastric cancer, the molecular mechanisms of gastric cancer cells in response to melatonin remains to be determined.

methodsThe SGC-7901 gastric cancer cells were treated with different concentrations of melatonin for 24 and 48 h. Cell viability was determined by MTT assay, Hoechst 33258 staining and FACS analysis were used to detect apoptotic cells. The contents and activation of apoptosis-related proteins HSP27, Akt and P38 were evaluated by immunoblotting analysis. Then we treated SGC-7901 cells with HSP27-specific siRNA, PI3K inhibitor LY294002 or P38 inhibitor SB203580 to investigate the role of HSP27, Akt and P38 in the anti-apoptotic response of SGC-7901 cells to melatonin.

resultsMelatonin suppressed cell viability and stimulated apoptosis of gastric cancer SGC-7901 cells dose-dependently. Mechanistically, the observed apoptosis was accompanied by the melatonin-induced phosphorylation of HSP27. HSP27-specific siRNA transfection effectively reduced HSP27 phosphorylation and augmented melatonin-induced apoptosis, indicating that HSP27 is resistant to melatonin-induced apoptosis. Moreover, melatonin increased PI3K/Akt activation, LY294002 abrogated HSP27 activation and promoted cell apoptosis induced by melatonin. Furthermore, melatonin increased P38 activity, and P38 inhibitor SB203580 inhibited melatonin-induced PI3K/Akt, HSP27 activation and accelerated cell apoptosis.

conclusionIn contrast to the well-established anti-cancer properties of melatonin, our study revealed clearly a distinguishable anti-apoptotic pathway induced by melatonin, that is, HSP27 plays a crucial role in apoptotic resistance in melatonin-treated gastric cancer cells, and its activation is most likely via the activation of P38/PI3K/Akt signaling.

Indexed as

Gastric cancerHSP27MelatoninP38PI3K/Akt

Identifiers

PMID26877709
PMCPMC4751649
OpenAlexW2253311583

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.