Evidence map›Paper›PMID 23203057›Full record

ArticleInternational journal of molecular sciences2012

Apoptosis induction of human prostate carcinoma DU145 cells by diallyl disulfide via modulation of JNK and PI3K/AKT signaling pathways.

Dong Yeok Shin, Gi-Young Kim, Jun Hyuk Lee, Byung Tae Choi, Young Hyun Yoo, Yung Hyun Choi

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Diallyl disulfide in oncotherapy: molecular mechanisms and therapeutic potentials.Apoptosis : an international journal on programmed cell death · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Anti-Tumor Effects of Heat-KilledMicroorganisms · 2022
    Article
  9. Review
  10. Article
  11. Role of Phytochemicals in Cancer Chemoprevention: Insights.Antioxidants (Basel, Switzerland) · 2021
    Review
  12. Observational
  13. Article
  14. Article
  15. Diallyl disulfide induces apoptosis and autophagy via mTOR pathway in myeloid leukemic cell line.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  16. Induced neural stem cells protect neuronal cells against apoptosis.Medical science monitor : international medical journal of experimental and clinical research · 2014
    Article
  17. Article
  18. Article
  19. Article
  20. Green tea polyphenols protect PC12 cells against HInternational journal of immunopathology and pharmacology
    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

6 authors at 6 institutions in 1 country.

Dong Yeok ShinDongnam Institute of Radiological & Medicine Sciences, Busan 619-953, Korea. yhyoo@dau.ac.kr.
Gi-Young Kim
Jun Hyuk Lee
Byung Tae Choi
Young Hyun Yoo
Yung Hyun Choi
Dong-A University · KRDong-Eui University · KRDongnam Institute of Radiological & Medical Sciences · KRJeju National University · KRKorean Intellectual Property Office · KRPusan National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diallyl disulfide (DADS), a sulfur compound derived from garlic, has various biological properties, such as anticancer, antiangiogenic and anti-inflammatory effects. However, the mechanisms of action underlying the compound's anticancer activity have not been fully elucidated. In this study, the apoptotic effects of DADS were investigated in DU145 human prostate carcinoma cells. Our results showed that DADS markedly inhibited the growth of the DU145 cells by induction of apoptosis. Apoptosis was accompanied by modulation of Bcl-2 and inhibitor of apoptosis protein (IAP) family proteins, depolarization of the mitochondrial membrane potential (MMP, ΔΨm) and proteolytic activation of caspases. We also found that the expression of death-receptor 4 (DR4) and Fas ligand (FasL) proteins was increased and that the level of intact Bid proteins was down-regulated by DADS. Moreover, treatment with DADS induced phosphorylation of mitogen-activated protein kinases (MAPKs), including extracellular-signal regulating kinase (ERK), p38 MAPK and c-Jun N-terminal kinase (JNK). A specific JNK inhibitor, SP600125, significantly blocked DADS-induced-apoptosis, whereas inhibitors of the ERK (PD98059) and p38 MAPK (SB203580) had no effect. The induction of apoptosis was also accompanied by inactivation of phosphatidylinositol 3-kinase (PI3K)/Akt and the PI3K inhibitor LY29004 significantly increased DADS-induced cell death. These findings provide evidence demonstrating that the proapoptotic effect of DADS is mediated through the activation of JNK and the inhibition of the PI3K/Akt signaling pathway in DU145 cells.

Indexed as

Allyl CompoundsApoptosisApoptosis Regulatory ProteinsCaspasesCell Line, TumorCell SurvivalDisulfidesEnzyme ActivationGene Expression Regulation, NeoplasticHumansJNK Mitogen-Activated Protein KinasesMaleMatrix MetalloproteinasesPhosphatidylinositol 3-KinasesProstatic NeoplasmsProto-Oncogene Proteins c-aktAllyl CompoundsApoptosis Regulatory ProteinsCaspasesdiallyl disulfideDisulfidesJNK Mitogen-Activated Protein KinasesMatrix MetalloproteinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID23203057
PMCPMC3509573
OpenAlexW1995437219

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.