Evidence map›Paper›PMID 31817791›Full record

ArticleBiomolecules2019

Benzyl Isothiocyanate Induces Apoptosis via Reactive Oxygen Species-Initiated Mitochondrial Dysfunction and DR4 and DR5 Death Receptor Activation in Gastric Adenocarcinoma Cells.

Khin Wah Wah Han, Wah Wah Po, Uy Dong Sohn, Hyun-Jung Kim

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2019. 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
1.9field-weighted citation impact, top 13% 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, 45 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Anticarcinogenic Effects of Isothiocyanates on Hepatocellular Carcinoma.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Hydrogen Sulfide Biology and Its Role in Cancer.Molecules (Basel, Switzerland) · 2022
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Transcriptomic Analysis, Motility and Biofilm Formation Characteristics ofInternational journal of molecular sciences · 2020
    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

4 authors at 1 institution in 1 country.

Khin Wah Wah HanCell Signaling and Pharmacological Activity Lab, Department of Pharmacology, College of Pharmacy, Chung-Ang University, Seoul 06974, Korea.
Wah Wah PoCell Signaling and Pharmacological Activity Lab, Department of Pharmacology, College of Pharmacy, Chung-Ang University, Seoul 06974, Korea.
Uy Dong SohnCell Signaling and Pharmacological Activity Lab, Department of Pharmacology, College of Pharmacy, Chung-Ang University, Seoul 06974, Korea.
Hyun-Jung KimNeuropharmacology and Stem Cell Lab, Department of Pharmacology, College of Pharmacy, Chung-Ang University, Seoul 06974, Korea.
Chung-Ang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Benzyl isothiocyanate (BITC) is known to inhibit the metastasis of gastric cancer cells but further studies are needed to confirm its chemotherapeutic potential against gastric cancer. In this study, we observed cell shrinkage and morphological changes in one of the gastric adenocarcinoma cell lines, the AGS cells, after BITC treatment. We performed 3-(4,5-dimethyl-2-thiazolyl)-2,5- diphenyl-2H-tetrazolium bromide (MTT) assay, a cell viability assay, and found that BITC decreased AGS cell viability. Reactive oxygen species (ROS) analyses using 2',7'-dichlorofluorescin diacetate (DCFDA) revealed that BITC-induced cell death involved intracellular ROS production, which resulted in mitochondrial dysfunction. Additionally, cell viability was partially restored when BITC-treated AGS cells were preincubated with glutathione (GSH). Western blotting indicated that BITC regulated the expressions of the mitochondria-mediated apoptosis signaling molecules, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), and cytochrome c (Cyt c). In addition, BITC increased death receptor DR5 expression, and activated the cysteine-aspartic proteases (caspases) cascade. Overall, our results showed that BITC triggers apoptosis in AGS cells via the apoptotic pathways involved in ROS-promoted mitochondrial dysfunction and death receptor activation.

Indexed as

AdenocarcinomaAntineoplastic AgentsApoptosisbcl-2-Associated X ProteinBiological ProductsCell DeathCell Line, TumorCell SurvivalCytochromes cHumansIsothiocyanatesMitochondriaProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesReceptors, TNF-Related Apoptosis-Inducing LigandSignal TransductionAntineoplastic Agentsbcl-2-Associated X Proteinbenzyl isothiocyanateBiological ProductsCytochromes cIsothiocyanatesProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesReceptors, TNF-Related Apoptosis-Inducing LigandTNFRSF10A protein, humanTNFRSF10B protein, humanapoptosisbenzyl isothiocyanatedeath receptorsgastric cancernatural productreactive oxygen species

Identifiers

PMID31817791
PMCPMC6995572
OpenAlexW2993497027

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.