Evidence map›Paper›PMID 28302032›Full record

ArticleCurrent cancer drug targets2017

Anti-Tumorigenic Effects of Resveratrol in Lung Cancer Cells Through Modulation of c-FLIP.

Clayton Wright, Anand Krishnan V Iyer, Juan S Yakisich, Neelam Azad

Abstract read
In one paragraph

Article in Current cancer drug targets, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
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  7. Review
  8. Molecular pharmacology · 2022
    Article
  9. Review
  10. Natural Compounds as Promising Adjuvant Agents in The Treatment of Gliomas.International journal of molecular sciences · 2022
    Review
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  13. Article
  14. Article
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  16. Review
  17. Article
  18. Exploring the anticancer potential ofJournal of advanced pharmaceutical technology & research
    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.

Clayton WrightDepartment of Pharmaceutical Sciences, Hampton University, Hampton, VA 23668. United States.
Anand Krishnan V IyerDepartment of Pharmaceutical Sciences, Hampton University, Hampton, VA 23668. United States.
Juan S YakisichDepartment of Pharmaceutical Sciences, Hampton University, Hampton, VA 23668. United States.
Neelam AzadDepartment of Pharmaceutical Sciences, Hampton University, Hampton, VA 23668. United States.
Hampton University · US

Funding

Anti-Tumorigenic Potential of Novel Digitoxin AnaloguesSC1CA173069 · NCI · HAMPTON UNIVERSITY · PI IYER, ANAND K. · 2012 to 2016
$1.3M
Impact of Oxidative Stress-Regulated Angiogenesis in Pulmonary FibrosisSC1HL112630 · NHLBI · HAMPTON UNIVERSITY · PI AZAD, NEELAM · 2011 to 2015
$1.3M
NCI NIH HHS SC1 CA173069NHLBI NIH HHS SC1 HL112630
6 · The paper itself

Abstract

backgroundResveratrol has been shown to have antioxidant and anti-proliferative properties in multiple cancer types. Here we demonstrate that H460 lung cancer cells are more susceptible to resveratrol treatment in comparison to human bronchial epithelial Beas-2B cells. Resveratrol decreases cell viability and proliferation, and induces significant apoptosis in H460 cells. The apoptosis observed was accompanied by an increase in hydrogen peroxide (H2O2) production, Bid, PARP and caspase 8 activation, and downregulation of pEGFR, pAkt, c-FLIP and NFkB protein expression. Furthermore, treatment with HH2O2 scavenger catalase significantly inhibited resveratrol-induced c-FLIP downregulation, caspase-8 activation and apoptosis. Overexpression of c-FLIP in H460 cells (FLIP cells) resulted in the inhibition of resveratrol-induced HH2O2 production, and a significant increase in resveratrolinduced apoptosis in comparison to H460 cells. In FLIP cells, catalase treatment did not rescue cells from a decrease in cell viability and apoptosis induction by resveratrol as compared to H460 cells. Resveratrol treatment also led to VEGF downregulation in FLIP cells. Furthermore, inhibition of pEGFR or pAkt using erlotinib and LY294002 respectively, enhanced the negative effect of resveratrol on FLIP cell viability and apoptosis. The reverse was observed when FLIP cells were supplemented with EGF, or transfected with WT-AKT plasmid; resulting in a 20% decrease in resveratrol-induced apoptosis. In addition, transfection with WT-AKT plasmid resulted in the inhibition of pro-apoptotic protein activation, and c-FLIP and pAkt downregulation.

conclusionOverall, resveratrol induced apoptosis in H460 lung cancer cells by specifically targeting pAkt and c-FLIP dowregulation by proteasomal degradation in a EGFR-dependent manner.

Indexed as

Antineoplastic Agents, PhytogenicApoptosisApoptosis Regulatory ProteinsCASP8 and FADD-Like Apoptosis Regulating ProteinCell Line, TumorHumansHydrogen PeroxideLung NeoplasmsProto-Oncogene Proteins c-aktReactive Oxygen SpeciesResveratrolStilbenesAntineoplastic Agents, PhytogenicApoptosis Regulatory ProteinsCASP8 and FADD-Like Apoptosis Regulating ProteinCFLAR protein, humanHydrogen PeroxideProto-Oncogene Proteins c-aktReactive Oxygen SpeciesResveratrolStilbenesAktapoptosisc-FLIPhydrogen peroxideLung cancerresveratrol

Identifiers

PMID28302032
PMCPMC6476192
OpenAlexW2595080131

What OpenQuestion holds

Textmetadata
LicenceTDM
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.