Evidence map›Paper›PMID 41799034›Full record

ArticleBioMedicine2026

Decyl caffeate inhibits the proliferation of human triple negative breast cancer cells.

Che-Yi Chao, Woei-Cheang Shyu, Chih-Lung Lin, En-Pei Isabel Chiang, Yueh-Hsiung Kuo, Feng-Yao Tang

Abstract read
In one paragraph

Article in BioMedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Che-Yi Chao *Department of Food Nutrition and Health Biotechnology, Asia University, Taichung 41354, Taiwan.
Woei-Cheang Shyu *Graduate Institute of Biomedical Science, China Medical University, Taichung 40604, Taiwan.
Chih-Lung LinDepartment of Neurosurgery, Asia University Hospital, Taichung 41354, Taiwan.
En-Pei Isabel ChiangDepartment of Food Science and Biotechnology, National Chung Hsing University, Taichung 402, Taiwan.
Yueh-Hsiung KuoDepartment of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung 40604, Taiwan.
Feng-Yao TangBiomedical Science Laboratory, Department of Nutrition, China Medical University, Taichung 40604, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Over recent decades, considerable attention has been directed toward the discovery of novel compounds capable of targeting survival-related signaling networks as therapeutic candidates for triple-negative breast cancer (TNBC). Central to TNBC pathobiology are the Akt/mTOR and MAPK/ERK signaling axes, both contribute to tumor progression and therapeutic resistance. Caffeic acid (CA), a naturally derived phenolic compound with anti-inflammatory activity, has previously been investigated for its anti-cancer potential. Purpose: In the present study, we explored the therapeutic value of newly synthesized CA derivatives in TNBC models using both cellular and animal based systems. Methods: The anti-tumor efficacy of these CA derivatives was examined through a series of functional assays, including cell proliferation, clonogenicity, cell cycle profiling, apoptosis quantification, ELISA, western blotting, and histopathological analysis. Results: Among the tested derivatives, decyl caffeate (DC) demonstrated the most pronounced inhibitory effects on TNBC cell growth, significantly decreasing viability, colony formation, and enhancing cisplatin responsiveness ( Conclusion: Altogether, these results highlight DC as a promising bioactive compound that targets essential oncogenic pathways in TNBC and support its potential for further preclinical development.

Indexed as

ApoptosisCell cycle arrestCell signalingDecyl caffeateTriplenegative breast cancer

Identifiers

PMID41799034
PMCPMC12962762

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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 OpenQuestion graph.