Evidence map›Paper›PMID 27875298›Full record

ArticleThe Journal of biological chemistry2016

Benzyl Isothiocyanate (BITC) Induces Reactive Oxygen Species-dependent Repression of STAT3 Protein by Down-regulation of Specificity Proteins in Pancreatic Cancer.

Ravi Kasiappan, Indira Jutooru, Keshav Karki, Erik Hedrick, Stephen Safe

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.2field-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

31 citing papers in PubMed, 48 citations in OpenAlex.

  1. Metabolite Variations inFood science & nutrition · 2026
    Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Specificity Proteins (Sp) and Cancer.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Hydrogen Sulfide Biology and Its Role in Cancer.Molecules (Basel, Switzerland) · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Inhibition of Growth of Colon Tumors and Proliferation of HT-29 Cells byOxidative medicine and cellular longevity · 2021
    Article
  15. Review
  16. Review
  17. Article
  18. Bioactivation of Napabucasin Triggers Reactive Oxygen Species-Mediated Cancer Cell Death.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Ravi KasiappanFrom the Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Texas 77843-4466.
Indira JutooruFrom the Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Texas 77843-4466.
Keshav KarkiFrom the Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Texas 77843-4466.
Erik HedrickFrom the Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Texas 77843-4466.
Stephen SafeFrom the Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Texas 77843-4466 ssafe@cvm.tamu.edu.
Texas A&M University · US

Funding

TARGETED GENOMICS FACILITY COREP30ES023512 · NIEHS · TEXAS A&M AGRILIFE RESEARCH · PI THREADGILL, DAVID W. · 2014 to 2017
$3.3M
NIEHS NIH HHS P30 ES023512
6 · The paper itself

Abstract

The antineoplastic agent benzyl isothiocyanate (BITC) acts by targeting multiple pro-oncogenic pathways/genes, including signal transducer and activator of transcription 3 (STAT3); however, the mechanism of action is not well known. As reported previously, BITC induced reactive oxygen species (ROS) in Panc1, MiaPaCa2, and L3.6pL pancreatic cancer cells. This was accompanied by induction of apoptosis and inhibition of cell growth and migration, and these responses were attenuated in cells cotreated with BITC plus glutathione (GSH). BITC also decreased expression of specificity proteins (Sp) Sp1, Sp3, and Sp4 transcription factors (TFs) and several pro-oncogenic Sp-regulated genes, including STAT3 and phospho-STAT3 (pSTAT3), and GSH attenuated these responses. Knockdown of Sp TFs by RNA interference also decreased STAT3/pSTAT3 expression. BITC-induced ROS activated a cascade of events that included down-regulation of c-Myc, and it was also demonstrated that c-Myc knockdown decreased expression of Sp TFs and STAT3 These results demonstrate that in pancreatic cancer cells, STAT3 is an Sp-regulated gene that can be targeted by BITC and other ROS inducers, thereby identifying a novel therapeutic approach for targeting STAT3.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBlotting, WesternCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansIsothiocyanatesMiceMice, NudePancreatic NeoplasmsReactive Oxygen SpeciesReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerAntineoplastic Agentsbenzyl isothiocyanateIsothiocyanatesReactive Oxygen SpeciesRNA, MessengerSp Transcription FactorsSTAT3 protein, humanSTAT3 Transcription FactorMyc (c-Myc)pancreatic cancerreactive oxygen species (ROS)specificity protein 1 (Sp1)STAT3

Identifiers

PMID27875298
PMCPMC5207142
OpenAlexW2562555293

What OpenQuestion holds

Textmetadata
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.