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Inhibition of Autophagy and the Cytoprotective Role of Smac Mimetic against ROS-Induced Cancer: A Potential Therapeutic Strategy in Relapse and Chemoresistance Cases in Breast Cancer
With more than a million deaths each year, breast cancer is the top cause of death in women. Around 70% of breast cancers are hormonally responsive. Although several therapeutic options exist, cancer resistance and recurrence render them inefficient and insufficient. The major key reason behind this...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10378261/ https://www.ncbi.nlm.nih.gov/pubmed/37504279 http://dx.doi.org/10.3390/cimb45070363 |
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author | Rafat, Sahar Hakami, Mohammed Ageeli Hazazi, Ali Alsaiari, Ahad Amer Rashid, Summya Hasan, Mohammad Raghibul Aloliqi, Abdulaziz A. Eisa, Alaa Abdulaziz Dar, Mohammad Irfan Khan, Mohd Faisal Dev, Kapil |
author_facet | Rafat, Sahar Hakami, Mohammed Ageeli Hazazi, Ali Alsaiari, Ahad Amer Rashid, Summya Hasan, Mohammad Raghibul Aloliqi, Abdulaziz A. Eisa, Alaa Abdulaziz Dar, Mohammad Irfan Khan, Mohd Faisal Dev, Kapil |
author_sort | Rafat, Sahar |
collection | PubMed |
description | With more than a million deaths each year, breast cancer is the top cause of death in women. Around 70% of breast cancers are hormonally responsive. Although several therapeutic options exist, cancer resistance and recurrence render them inefficient and insufficient. The major key reason behind this is the failure in the regulation of the cell death mechanism. In addition, ROS was also found to play a major role in this problem. The therapeutic benefits of Smac mimetic compound (SMC) BV6 on MCF7 were examined in the current study. Treatment with BV6 reduces viability and induces apoptosis in MCF7 breast cancer cells. BV6 suppresses autophagy and has demonstrated a defensive role in cancer cells against oxidative stress caused by H(2)O(2). Overall, the present investigation shows that SMC has therapeutic and cytoprotective potential against oxidative stress in cancer cells. These Smac mimetic compounds may be used as anti-cancer drugs as well as antioxidants alone or in conjunction with other commonly used antioxidants. |
format | Online Article Text |
id | pubmed-10378261 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-103782612023-07-29 Inhibition of Autophagy and the Cytoprotective Role of Smac Mimetic against ROS-Induced Cancer: A Potential Therapeutic Strategy in Relapse and Chemoresistance Cases in Breast Cancer Rafat, Sahar Hakami, Mohammed Ageeli Hazazi, Ali Alsaiari, Ahad Amer Rashid, Summya Hasan, Mohammad Raghibul Aloliqi, Abdulaziz A. Eisa, Alaa Abdulaziz Dar, Mohammad Irfan Khan, Mohd Faisal Dev, Kapil Curr Issues Mol Biol Article With more than a million deaths each year, breast cancer is the top cause of death in women. Around 70% of breast cancers are hormonally responsive. Although several therapeutic options exist, cancer resistance and recurrence render them inefficient and insufficient. The major key reason behind this is the failure in the regulation of the cell death mechanism. In addition, ROS was also found to play a major role in this problem. The therapeutic benefits of Smac mimetic compound (SMC) BV6 on MCF7 were examined in the current study. Treatment with BV6 reduces viability and induces apoptosis in MCF7 breast cancer cells. BV6 suppresses autophagy and has demonstrated a defensive role in cancer cells against oxidative stress caused by H(2)O(2). Overall, the present investigation shows that SMC has therapeutic and cytoprotective potential against oxidative stress in cancer cells. These Smac mimetic compounds may be used as anti-cancer drugs as well as antioxidants alone or in conjunction with other commonly used antioxidants. MDPI 2023-07-10 /pmc/articles/PMC10378261/ /pubmed/37504279 http://dx.doi.org/10.3390/cimb45070363 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Rafat, Sahar Hakami, Mohammed Ageeli Hazazi, Ali Alsaiari, Ahad Amer Rashid, Summya Hasan, Mohammad Raghibul Aloliqi, Abdulaziz A. Eisa, Alaa Abdulaziz Dar, Mohammad Irfan Khan, Mohd Faisal Dev, Kapil Inhibition of Autophagy and the Cytoprotective Role of Smac Mimetic against ROS-Induced Cancer: A Potential Therapeutic Strategy in Relapse and Chemoresistance Cases in Breast Cancer |
title | Inhibition of Autophagy and the Cytoprotective Role of Smac Mimetic against ROS-Induced Cancer: A Potential Therapeutic Strategy in Relapse and Chemoresistance Cases in Breast Cancer |
title_full | Inhibition of Autophagy and the Cytoprotective Role of Smac Mimetic against ROS-Induced Cancer: A Potential Therapeutic Strategy in Relapse and Chemoresistance Cases in Breast Cancer |
title_fullStr | Inhibition of Autophagy and the Cytoprotective Role of Smac Mimetic against ROS-Induced Cancer: A Potential Therapeutic Strategy in Relapse and Chemoresistance Cases in Breast Cancer |
title_full_unstemmed | Inhibition of Autophagy and the Cytoprotective Role of Smac Mimetic against ROS-Induced Cancer: A Potential Therapeutic Strategy in Relapse and Chemoresistance Cases in Breast Cancer |
title_short | Inhibition of Autophagy and the Cytoprotective Role of Smac Mimetic against ROS-Induced Cancer: A Potential Therapeutic Strategy in Relapse and Chemoresistance Cases in Breast Cancer |
title_sort | inhibition of autophagy and the cytoprotective role of smac mimetic against ros-induced cancer: a potential therapeutic strategy in relapse and chemoresistance cases in breast cancer |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10378261/ https://www.ncbi.nlm.nih.gov/pubmed/37504279 http://dx.doi.org/10.3390/cimb45070363 |
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