What question did this study set out to answer?

The aim is to evaluate the effects of decyl caffeate on the growth of triple-negative breast cancer cells and understand its underlying mechanisms.

February 28, 2026Open Access

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

Key Points

The aim is to evaluate the effects of decyl caffeate on the growth of triple-negative breast cancer cells and understand its underlying mechanisms.
Functional assays including cell proliferation and apoptosis quantification were conducted.
Western blotting and histopathological analyses were performed to assess molecular changes.
Murine TNBC xenograft model was used for in vivo evaluation of decyl caffeate.
Decyl caffeate significantly reduced viability and colony formation in TNBC cells.
It caused G2/M phase arrest and downregulated cyclin B1 and CDK1.
Colony formation and apoptosis markers like Bax and cleaved caspase-3 were upregulated.
Oral administration of decyl caffeate suppressed tumor growth in mice.

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 (P < 0.05). DC induced G2/M phase arrest in MDA-MB-468 cells, accompanied by suppression of cyclin B1 and CDK1 expression. In addition, DC downregulated both total and phosphorylated c- Myc and reduced secretion of TGF-α, a key ligand for EGFR. Apoptotic responses were evident through upregulation of Bax, cleaved caspase-3, and cleaved-PARP. Mechanistic analysis revealed that these effects were mediated via concurrent inactivation of the Akt/mTOR and MAPK/ERK signaling pathways. Oral administration of DC in a murine TNBC xenograft model significantly suppressed tumor growth in vivo. 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.

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