Evidence map›Paper›PMID 12894226›Full record

ArticleOncogene2003

Role of p53 and NF-kappaB in epigallocatechin-3-gallate-induced apoptosis of LNCaP cells.

Kedar Hastak, Sanjay Gupta, Nihal Ahmad, Mukesh K Agarwal, Munna L Agarwal, Hasan Mukhtar

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed
13.7field-weighted citation impact, top 1% 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

105 citing papers in PubMed, 325 citations in OpenAlex.

  1. Trial
  2. Article
  3. Stevia Leaf Extract Fermented with Plant-DerivedInternational journal of molecular sciences · 2025
    Article
  4. Review
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  6. Article
  7. Article
  8. Review
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  14. Article
  15. Article
  16. Article
  17. Article
  18. Prostate cancer: Therapeutic prospect with herbal medicine.Current research in pharmacology and drug discovery · 2021
    Review
  19. Review
  20. Review

45 more citing papers are in PubMed but not listed here.

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

6 authors at 4 institutions in 1 country.

Kedar HastakDepartment of Environmental Health Sciences, Case Western Reserve University, Cleveland, OH 44106, USA.
Sanjay Gupta
Nihal Ahmad
Mukesh K Agarwal
Munna L Agarwal
Hasan Mukhtar
Cleveland Clinic · USUniversity of Wisconsin–Madison · USCase Western Reserve University · USUniversity Hospitals of Cleveland · US

Funding

Green Tea in Chemoprevention of Prostate CancerR01CA078809 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI MUKHTAR, HASAN · 1999 to 2008
$1.9M
NCI NIH HHS R01 CA 78809
6 · The paper itself

Abstract

We have recently shown that oral consumption of green tea polyphenols inhibits prostate carcinogenesis in transgenic mouse model of prostate cancer and suggested that induction of apoptosis in prostate cancer cells is responsible for these effects. Much of the chemopreventive effects of green tea are attributed to its major polyphenolic constituent (-) epigallocatechin-3-gallate (EGCG). In the present study, we report that EGCG-induced apoptosis in human prostate carcinoma LNCaP cells is mediated via modulation of two related pathways: (a) stabilization of p53 by phosphorylation on critical serine residues and p14ARF-mediated downregulation of murine double minute 2(MDM2) protein, and (b) negative regulation of NF-kappaB activity, thereby decreasing the expression of the proapoptotic protein Bcl-2. EGCG-induced stabilization of p53 caused an upregulation in its transcriptional activity, thereby resulting in activation of its downstream targets p21/WAF1 and Bax. Thus, EGCG had a concurrent effect on two important transcription factors p53 and NF-kappaB, causing a change in the ratio of Bax/Bcl-2 in a manner that favors apoptosis. This altered expression of Bcl-2 family members triggered the activation of initiator capsases 9 and 8 followed by activation of effector caspase 3. Activation of the caspases was followed by poly (ADP-ribose) polymerase cleavage and induction of apoptosis. Taken together, the data indicate that EGCG induces apoptosis in human prostate carcinoma cells by shifting the balance between pro- and antiapoptotic proteins in favor of apoptosis.

Indexed as

Nuclear ProteinsAdenocarcinomaAnticarcinogenic AgentsApoptosisbcl-2-Associated X ProteinCaspase 3Caspase 8Caspase 9CaspasesCatechinCell DivisionCyclin-Dependent Kinase Inhibitor p21CyclinsDNA, NeoplasmEnzyme ActivationGene Expression Regulation, NeoplasticAnticarcinogenic AgentsBAX protein, humanbcl-2-Associated X ProteinCASP3 protein, humanCasp3 protein, mouseCASP8 protein, humanCasp8 protein, mouseCASP9 protein, humanCasp9 protein, mouseCaspase 3Caspase 8Caspase 9CaspasesCatechinCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21CyclinsDNA, Neoplasmepigallocatechin gallateMDM2 protein, humanNeoplasm ProteinsNF-kappa BNuclear ProteinsPoly(ADP-ribose) PolymerasesProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p14ARFTumor Suppressor Protein p53

Identifiers

PMID12894226
OpenAlexW2036809593

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.