Evidence map›Paper›PMID 14979919›Full record

ArticleBreast cancer research : BCR2004

Antiproliferative and apoptotic effects of selective phenolic acids on T47D human breast cancer cells: potential mechanisms of action.

Marilena Kampa, Vassilia-Ismini Alexaki, George Notas, Artemissia-Phoebe Nifli, Anastassia Nistikaki, Anastassia Hatzoglou, Efstathia Bakogeorgou, Elena Kouimtzoglou, George Blekas, Dimitrios Boskou and 2 more

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

79 citing papers in PubMed, 402 citations in OpenAlex.

  1. Review
  2. LC-ESI-MS/MS Analysis ofMolecules (Basel, Switzerland) · 2026
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  16. Catechins and Proanthocyanidins Involvement in Metabolic Syndrome.International journal of molecular sciences · 2023
    Review
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  18. Review
  19. Review
  20. Antihyaluronidase and Antioxidant Potential ofMolecules (Basel, Switzerland) · 2023
    Article

19 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

12 authors at 2 institutions in 1 country.

Marilena KampaLaboratory of Experimental Endocrinology, University of Crete, Heraklion, Greece.
Vassilia-Ismini Alexaki
George Notas
Artemissia-Phoebe Nifli
Anastassia Nistikaki
Anastassia Hatzoglou
Efstathia Bakogeorgou
Elena Kouimtzoglou
George Blekas
Dimitrios Boskou
Achille Gravanis
Elias Castanas
University of Crete · GRAristotle University of Thessaloniki · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe oncoprotective role of food-derived polyphenol antioxidants has been described but the implicated mechanisms are not yet clear. In addition to polyphenols, phenolic acids, found at high concentrations in a number of plants, possess antioxidant action. The main phenolic acids found in foods are derivatives of 4-hydroxybenzoic acid and 4-hydroxycinnamic acid.

methodsThis work concentrates on the antiproliferative action of caffeic acid, syringic acid, sinapic acid, protocatechuic acid, ferulic acid and 3,4-dihydroxy-phenylacetic acid (PAA) on T47D human breast cancer cells, testing their antioxidant activity and a number of possible mechanisms involved (interaction with membrane and intracellular receptors, nitric oxide production).

resultsThe tested compounds showed a time-dependent and dose-dependent inhibitory effect on cell growth with the following potency: caffeic acid > ferulic acid = protocatechuic acid = PAA > sinapic acid = syringic acid. Caffeic acid and PAA were chosen for further analysis. The antioxidative activity of these phenolic acids in T47D cells does not coincide with their inhibitory effect on tumoral proliferation. No interaction was found with steroid and adrenergic receptors. PAA induced an inhibition of nitric oxide synthase, while caffeic acid competes for binding and results in an inhibition of aryl hydrocarbon receptor-induced CYP1A1 enzyme. Both agents induce apoptosis via the Fas/FasL system.

conclusionsPhenolic acids exert a direct antiproliferative action, evident at low concentrations, comparable with those found in biological fluids after ingestion of foods rich in phenolic acids. Furthermore, the direct interaction with the aryl hydrocarbon receptor, the nitric oxide synthase inhibition and their pro-apoptotic effect provide some insights into their biological mode of action.

Indexed as

ApoptosisBreast NeoplasmsCell CycleCell Line, TumorCell ProliferationDose-Response Relationship, DrugHumansHydroxybenzoatesReceptors, Aryl HydrocarbonTime FactorsHydroxybenzoatesphenolic acidReceptors, Aryl Hydrocarbon

Identifiers

PMID14979919
PMCPMC400651
OpenAlexW1830337001

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.