Evidence map›Paper›PMID 41569314›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2026

Anti-cancer effects of carvacrol on NUF2, CASP3 and CLDN6 expression in T47D breast cancer cells.

Emir Nekay, Asmaa Abuaisha

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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

2 authors.

Emir NekayDepartment of General Surgery, Faculty of Medicine, Biruni University, Istanbul, Turkey. nekayemir@hotmail.com.
Asmaa AbuaishaBiruni University Advanced Technology and Research Center B@MER, Biruni University, Istanbul, Turkey. asmaa.m.abuaisha@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer (BC) remains a major global health challenge, with rising incidence and mortality despite advances in diagnosis and treatment. Identifying new therapeutic agents targeting key molecular pathways is critical for improving patient outcomes. This study investigated the anticancer potential of carvacrol, a natural monoterpenoid phenol, in T47D luminal A BC cells, focusing on its effects on cell viability, migration, oxidative stress, and the expression of NUF2, CASP3 and CLDN6. T47D cells were treated with 480 µM carvacrol for 48 h. Cell viability, wound healing assay, intracellular reactive oxygen species (ROS) levels assay and gene expression were evaluated. Carvacrol significantly inhibited cell viability and reduced wound closure compared with controls. It markedly decreased intracellular ROS levels, indicating modulation of cellular redox status. Gene expression analysis revealed a significant downregulation of NUF2 (P < 0.01) and upregulation of both CASP3 (P < 0.01) and CLDN6 (P < 0.001). These findings suggest that carvacrol treatment is associated with transcriptional changes in genes related to proliferation, apoptosis, and cell junction dynamics. Carvacrol exhibits anticancer-related effects in T47D luminal A BC cells by altering cell viability, migration, oxidative stress, and the expression of NUF2, CASP3, and CLDN6. While these results highlight carvacrol's multi-targeted transcriptional impact, further studies are required to clarify the underlying molecular mechanisms and functional consequences.

Indexed as

Antineoplastic AgentsBreast NeoplasmsCaspase 3ClaudinsCymenesMonoterpenesApoptosisCell Line, TumorCell MovementCell SurvivalFemaleGene Expression Regulation, NeoplasticHumansOxidative StressReactive Oxygen SpeciesAntineoplastic AgentscarvacrolCASP3 protein, humanCaspase 3claudin 6ClaudinsCymenesMonoterpenesReactive Oxygen SpeciesBreast cancerCarvacrolCASP3CLDN6NUF2Oxidative stress

Identifiers

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Registered trials

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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 Socratic graph.