Doxorubicin-Induced Modulation of NF-κB, Bcl-2, and Bax Expression in Breast Cancer Cell Lines.
Authors:
- Melissa BuitronMelissa Buitron
- Angeline Caprice Riera PerezAngeline Caprice Riera Perez
- Ariana Camila Zegarra BandaAriana Camila Zegarra Banda
- Elvis Gonzales-CondoriElvis Gonzales-Condori
- Jose Miguel Carpio CarpioJose Miguel Carpio Carpio
- Jose Antonio Villanueva-SalasJose Antonio Villanueva-Salas
- Celia Choquenaira-QuispeCelia Choquenaira-Quispe
Open Access
- 1 January 2025
- conference paper
- Published by LACCEI (Latin American and Caribbean Consortium of Engineering Institutions)
Abstract
Breast cancer is the most common malignancy and one of the leading causes of death in women worldwide. Breast cells grow uncontrollably, forming tumors that can spread through the blood or lymphatic system. The treatment of breast cancer includes surgery, radiotherapy and the use of drugs such as doxorubicin, which aim to reduce the size of the tumor and improve the patient's condition. However, their efficacy is limited due to factors such as cellular resistance and efflux transporter activity. The aim of the work was to analyze the expression of NF-kB, Bcl-2 and Bax in MCF-7 and MDA-MB-231 breast cancer cell lines treated with doxorubicin (DOX). IC50 analysis of DOX was performed by MTT assay, gene quantification was by qPCR and In silico analysis of TLR4 and DOX was performed. MTT results showed that the IC50 for MCF-7 and MDA-MB-231 were 0.1µM and 0.3µM respectively. The qPCR results showed that the overexpression of NF-κB was 1.825±0.054 and 10.85±1.000 in MDA-MB-231 and MCF-7 cell lines respectively. For Bax, the expression level was 1.827±0.1036 and 0.6869±0.092 in MDA-MB-231 and MCF-7 cell line consecutively. Furthermore, In silico analysis showed that DOX docks into the extracellular domain cavity of TLR4 through interactions with Lys52 and Ile65A residues.Keywords
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