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Adv Pharm Bull. 2024;14(3): 604-612.
doi: 10.34172/apb.2024.055
  Abstract View: 348
  PDF Download: 176

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Cytobiological Alterations Induced by Celecoxib as an Anticancer Agent for Breast and Metastatic Breast Cancer

Maher Monir. Akl 1* ORCID logo, Amr Ahmed 2 ORCID logo

1 Department of Chemistry, Faculty of Science, Mansoura University, 35516, Mansoura, Egypt.
2 The Public Health Department, Riyadh First Health Cluster, Ministry of Health, Saudi Arabia.
*Corresponding Author: Maher Monir. Akl, Email: maherakl555@gmail.com

Abstract

Breast cancer remains a formidable public health challenge worldwide, characterized by its initiation within the breast’s diverse tissues, particularly the ducts and lobules. This malignancy is predominantly categorized into three subtypes based on receptor status and genetic markers: hormone receptor-positive, HER2-positive, and triple-negative. Each subtype exhibits distinct biological behaviors and responses to treatment, which significantly influence the prognosis and management strategies. The development and metastatic spread of breast cancer are complex processes mediated by interactions between tumor cells and the host microenvironment, involving various cellular and molecular mechanisms. This review highlights the potential therapeutic role of celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, in addressing the multifaceted aspects of breast cancer progression. Specifically, celecoxib modulates angiogenesis by reducing the levels of vascular endothelial growth factor (VEGF) through decreased PGE2 production, enhances the immune response by alleviating PGE2-mediated immunosuppression, and inhibits metastasis by limiting the activity of matrix metalloproteinases (MMPs). These mechanisms collectively hinder tumor growth, immune evasion, and metastatic spread. By synthesizing recent findings and analyzing the impact of celecoxib on these pathways, this paper seeks to delineate the integrated approaches necessary for managing metastatic breast cancer effectively.
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Submitted: 21 Apr 2024
Revision: 20 Jun 2024
Accepted: 26 Jun 2024
ePublished: 29 Jun 2024
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