Evidence map›Paper›PMID 22266465›Full record

ArticleCarcinogenesis2012

Generation of reactive oxygen species by grape seed extract causes irreparable DNA damage leading to G2/M arrest and apoptosis selectively in head and neck squamous cell carcinoma cells.

Sangeeta Shrotriya, Gagan Deep, Mallikarjuna Gu, Manjinder Kaur, Anil K Jain, Swetha Inturi, Rajesh Agarwal, Chapla Agarwal

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.5field-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

23 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Antioxidant and Anticancer Activity ofLife (Basel, Switzerland) · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Role of oxidative stress in cytotoxicity of grape seed extract in human bladder cancer cells.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2013
    Article
  20. 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

8 authors at 4 institutions in 1 country.

Sangeeta ShrotriyaDepartment of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado, Aurora, CO 80045, USA.
Gagan Deep
Mallikarjuna Gu
Manjinder Kaur
Anil K Jain
Swetha Inturi
Rajesh Agarwal
Chapla Agarwal
University of Colorado Anschutz Medical Campus · USUniversity of Montana · USUniversity of Colorado Cancer Center · USUniversity of Colorado Denver · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Prostate Cancer Prevention by Procyanidins in Grape Seed ExtractR01CA091883 · NCI · UNIVERSITY OF COLORADO DENVER · PI AGARWAL, CHAPLA · 2003 to 2012
$3.3M
Colon Cancer Chemoprevention by Grape Seed ExtractR01AT003623 · NCCIH · UNIVERSITY OF COLORADO DENVER · PI AGARWAL, CHAPLA · 2007 to 2011
$1.9M
NCCIH NIH HHS R01 AT003623NCI NIH HHS CA91883NCI NIH HHS P30 CA046934
6 · The paper itself

Abstract

Head and neck squamous cell carcinoma (HNSCC) accounts for 6% of all malignancies in USA and unfortunately the recurrence of secondary primary tumors and resistance against conventional treatments decrease the overall 5 year survival rate in HNSCC patients. Thus, additional approaches are needed to control HNSCC. Here, for the first time, employing human HNSCC Detroit 562 and FaDu cells as well as normal human epidermal keratinocytes, we investigate grape seed extract (GSE) efficacy and associated mechanism in both cell culture and nude mice xenografts. GSE selectively inhibited the growth and caused cell cycle arrest and apoptotic death in both Detroit 562 and FaDu cells by activating DNA damage checkpoint cascade, including ataxia telangiectasia mutated/ataxia telangiectasia-Rad3-related-checkpoint kinase 1/2-cell division cycle 25C as well as caspases 8, 9 and 3. Consistent with these results, GSE treatment resulted in a strong DNA damage and a decrease in the levels of DNA repair molecules breast cancer gene 1 and Rad51 and DNA repair foci. GSE-caused accumulation of intracellular reactive oxygen species was identified as a major mechanism of its effect for growth inhibition, DNA damage and apoptosis, which was remarkably reversed by antioxidant N-acetylcysteine. GSE feeding to nude mice decreased Detroit 562 and FaDu xenograft tumor growth by 67 and 65% (P < 0.001), respectively. In immunohistochemical analysis, xenografts from GSE-fed groups showed decreased proliferation but increased DNA damage and apoptosis. Together, these findings show that GSE targets both DNA damage and repair and provide mechanistic insights for its efficacy selectively against HNSCC both in cell culture and mouse xenograft, supporting its translational potential against HNSCC.

Indexed as

DNA DamageAnimalsApoptosisCarcinoma, Squamous CellCell DivisionFluorescent Antibody TechniqueG2 PhaseHead and Neck NeoplasmsHumansMaleMiceMice, NudePlant ExtractsReactive Oxygen SpeciesSeedsTumor Cells, CulturedPlant ExtractsReactive Oxygen Species

Identifiers

PMID22266465
PMCPMC3324440
OpenAlexW2101607117

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.