Article3 Biotech2025
Synergistic targeting of cancer-related proteins by benzyl isothiocyanate and caffeic acid: MLSD and cytotoxic mechanisms in MCF-7 cells.
Article in 3 Biotech, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed.
- Recent Developments in Ferulic Acid- and Caffeic Acid-Based Hybrids with Potential Anticancer Properties.Molecules (Basel, Switzerland) · 2026Review
- Caffeic Acid and Human Health: Evidence-Based Roles in Disease Prevention and Treatment.International journal of molecular sciences · 2026Review
- Bio-functional and anti-cancer (MCF-7) benzyl isothiocyanate nanoemulsions preparation using green pressurized water and process optimization.Scientific reports · 2026Article
- Article
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Authors and funding
4 authors.
Funding
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Abstract
This study investigated the synergistic cytotoxic effects of benzyl isothiocyanate (BITC) and caffeic acid (CA) on human breast adenocarcinoma (MCF-7) cells. Cell viability assays (MTT) revealed that BITC induces reactive oxygen species (ROS)-mediated cell death, while CA alone exhibited minimal cytotoxicity. Notably, their combination selectively enhanced MCF-7 cell death with limited effects on human fibroblasts. Mechanistic investigations demonstrated MAPK pathway activation and apoptosis induction, supported by altered expression of GST, p38, p-ERK, ERK 1/2, Nrf-2, and Bcl-2 proteins. Fluorometric analysis revealed significant disruption of redox homeostasis, including changes in ROS, glutathione (GSH), and caspase-3/7 activity. Molecular docking studies confirmed stable binding interactions (binding energies: -4.9 to -6.8 kcal/mol) of BITC and CA with key cancer-related proteins (ERK2, p38 MAPK, Bcl-2, Keap1-Nrf2, GST). Furthermore, Multiple Ligand Simultaneous Docking (MLSD) demonstrated the cooperative binding of BITC and CA to shared and distinct residues within the same protein targets, revealing enhanced binding affinity and potential synergistic inhibition of oncogenic pathways. These results highlight the synergistic potential of BITC and CA to modulate the MAPK pathway, disrupt cellular homeostasis, and induce apoptosis, underscoring their promise for combination cancer therapy. Supplementary Information: The online version contains supplementary material available at 10.1007/s13205-025-04469-1.
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