Investigation of the molecular mechanisms of action of sophorolipids in MCF-7 cells: therapeutic potential against breast cancer.
- 1Department of General Biology, State University of Londrina, Londrina, Paraná Brazil.
- 2Department of Biochemistry and Biotechnology, State University of Londrina, Londrina, Paraná Brazil.
Abstract
A mixture of lactonic and acidic sophorolipids exerted concentration-dependent cytotoxicity against human breast ductal adenocarcinoma (MCF-7) cells, with an IC₅₀ of 82.54 µg/mL as determined by resazurin assay. Phase-contrast microscopy revealed morphological alterations including cell swelling, loss of adhesion, and impaired membrane integrity. Flow cytometry analysis demonstrated cell cycle arrest in the S phase, mitochondrial membrane depolarization, and a predominance of necrosis-like cell death at higher concentrations. Transcriptional profiling by RT-qPCR identified overexpression of CDKN1A, GADD45A, ERN1, and BBC3, alongside repression of ACTB and GAPDH, indicating activation of DNA damage and stress-response pathways, endoplasmic reticulum stress, structural collapse, and metabolic dysfunction. Collectively, these findings demonstrate that sophorolipids induce mitochondrial and endoplasmic reticulum stress, culminating in homeostatic failure and cell death in MCF-7 cells, positioning these biosurfactants as promising candidates for the development of natural antiproliferative therapies.Supplementary information
The online version contains supplementary material available at https://doi.org/10.1007/s13205-026-05096-0.
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BibTeX
@article{martins2026investigation,
title = {{Investigation of the molecular mechanisms of action of sophorolipids in MCF-7 cells: therapeutic potential against breast cancer.}},
author = {Luiz Henrique Santana Martins and Luan Vitor Alves de Lima and Matheus Felipe da Silva and Niumaique Gonçalves da Silva and Maria Claudia Terkelli de Assis and Isabella Cristina Oliveira Carvalho and Isaura Maria Fuzzinato and Beatriz Braga Silva and Dimitri Alves da Costa and Mattheus Pizane de Azevedo Silva and Maria Antonia Pedrine Colabone Celligoi and Mario Sérgio Mantovani},
journal = {3 Biotech},
year = {2026},
month = oct,
doi = {10.1007/s13205-026-05096-0},
url = {https://europepmc.org/article/MED/42926778},
note = {CC BY},
}
RIS
TY - JOUR
TI - Investigation of the molecular mechanisms of action of sophorolipids in MCF-7 cells: therapeutic potential against breast cancer.
AU - Luiz Henrique Santana Martins
AU - Luan Vitor Alves de Lima
AU - Matheus Felipe da Silva
AU - Niumaique Gonçalves da Silva
AU - Maria Claudia Terkelli de Assis
AU - Isabella Cristina Oliveira Carvalho
AU - Isaura Maria Fuzzinato
AU - Beatriz Braga Silva
AU - Dimitri Alves da Costa
AU - Mattheus Pizane de Azevedo Silva
AU - Maria Antonia Pedrine Colabone Celligoi
AU - Mario Sérgio Mantovani
PY - 2026
DA - 2026/10/23
JO - 3 Biotech
DO - 10.1007/s13205-026-05096-0
UR - https://europepmc.org/article/MED/42926778
AB - A mixture of lactonic and acidic sophorolipids exerted concentration-dependent cytotoxicity against human breast ductal adenocarcinoma (MCF-7) cells, with an IC₅₀ of 82.54 µg/mL as determined by resazurin assay. Phase-contrast microscopy revealed morphological alterations including cell swelling, loss of adhesion, and impaired membrane integrity. Flow cytometry analysis demonstrated cell cycle arrest in the S phase, mitochondrial membrane depolarization, and a predominance of necrosis-like cell death at higher concentrations. Transcriptional profiling by RT-qPCR identified overexpression of CDKN1A, GADD45A, ERN1, and BBC3, alongside repression of ACTB and GAPDH, indicating activation of DNA damage and stress-response pathways, endoplasmic reticulum stress, structural collapse, and metabolic dysfunction. Collectively, these findings demonstrate that sophorolipids induce mitochondrial and endoplasmic reticulum stress, culminating in homeostatic failure and cell death in MCF-7 cells, positioning these biosurfactants as promising candidates for the development of natural antiproliferative therapies.Supplementary information The online version contains supplementary material available at https://doi.org/10.1007/s13205-026-05096-0.
SN - 2190-572X
SN - 2190-5738
ER -