Evidence map›Paper›PMID 28423628›Full record

ArticleOncotarget2017

Benzyl isothiocyanate induces reactive oxygen species-initiated autophagy and apoptosis in human prostate cancer cells.

Ji-Fan Lin, Te-Fu Tsai, Shan-Che Yang, Yi-Chia Lin, Hung-En Chen, Kuang-Yu Chou, Thomas I-Sheng Hwang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Direct Interaction betweenAntioxidants (Basel, Switzerland) · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. ROS-Mediated Cancer Cell Killing through Dietary Phytochemicals.Oxidative medicine and cellular longevity · 2019
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
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.

Ji-Fan LinCentral Laboratory, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, 111, Taiwan.
Te-Fu TsaiDivision of Urology, Department of Surgery, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, 111, Taiwan.
Shan-Che YangCentral Laboratory, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, 111, Taiwan.
Yi-Chia LinDivision of Urology, Department of Surgery, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, 111, Taiwan.
Hung-En ChenDivision of Urology, Department of Surgery, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, 111, Taiwan.
Kuang-Yu ChouDivision of Urology, Department of Surgery, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, 111, Taiwan.
Thomas I-Sheng HwangDivision of Urology, Department of Surgery, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, 111, Taiwan.
Fu Jen Catholic University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Benzyl isothiocyanate (BITC) in cruciferous plants, which are part of the human diet, has been shown to induce apoptosis in various types of cancer. In this study, we show that BITC effectively suppresses the growth of cultured human prostate cancer cells (CRW-22Rv1 and PC3) by causing mitochondrial membrane potential loss, caspase 3/7 activation and DNA fragmentation. Furthermore, BITC induces ROS generation in these cells. The induction of apoptosis by BITC was significantly attenuated in the presence of N-acetylcysteine (NAC) and catalase (CAT), well-studied ROS scavengers. The induction of autophagy in BITC-treated cells were also diminished by the application of NAC or CAT. In addition, BITC-induced apoptosis and autophagy were both enhanced by the pretreatment of catalase inhibitor, 3-Amino-1,2,4-triazole (3-AT). Pretreatment with specific inhibitors of autophagy (3-methyladenine or bafilomycin A1) or apoptosis (Z-VAD-FMK) reduced BITC-induced autophagy and apoptosis, respectively, but did not abolish BITC-induced ROS generation. In conclusion, the present study provides evidences that BITC caused prostate cancer cell death was dependent on the ROS status, and clarified the mechanism underlying BITC-induced cell death, which involves the induction of ROS production, autophagy and apoptosis, and the relationship between these three important processes.

Indexed as

Antineoplastic AgentsApoptosisAutophagyBlotting, WesternCell Line, TumorCell SurvivalFlow CytometryHumansIsothiocyanatesMaleMembrane Potential, MitochondrialProstatic NeoplasmsReactive Oxygen SpeciesAntineoplastic Agentsbenzyl isothiocyanateIsothiocyanatesReactive Oxygen Speciesapoptosisautophagybenzyl isothiocyanateprostate cancerreactive oxygen species

Identifiers

PMID28423628
PMCPMC5386757
OpenAlexW2589266856

What OpenQuestion holds

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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.