Targeting autophagy with tamoxifen in breast cancer: From molecular mechanisms to targeted therapy
- PMID: 37402635
- DOI: 10.1111/fcp.12936
Targeting autophagy with tamoxifen in breast cancer: From molecular mechanisms to targeted therapy
Abstract
Background: Tamoxifen (TAM) is often recommended as a first-line treatment for estrogen receptor-positive breast cancer (BC). However, TAM resistance continues to be a medical challenge for BC with hormone receptor positivity. The function of macro-autophagy and autophagy has recently been identified to be altered in BC, which suggests a potential mechanism for TAM resistance. Autophagy is a cellular stress-induced response to preserve cellular homeostasis. Also, therapy-induced autophagy, which is typically cytoprotective and activated in tumor cells, could sometimes be non-protective, cytostatic, or cytotoxic depending on how it is regulated.
Objective: This review explored the literature on the connections between hormonal therapies and autophagy. We investigated how autophagy could develop drug resistance in BC cells.
Methods: Scopus, Science Direct, PubMed, and Google Scholar were used to search articles for this study.
Results: The results demonstrated that protein kinases such as pAMPK, BAX, and p-p70S6K could be a sign of autophagy in developing TAM resistance. According to the study's findings, autophagy plays an important role in BC patients' TAM resistance.
Conclusion: Therefore, by overcoming endocrine resistance in estrogen receptor-positive breast tumors, autophagy inhibition may improve the therapeutic efficacy of TAM.
Keywords: anticancer properties; autophagy; breast cancer; tamoxifen.
© 2023 Société Française de Pharmacologie et de Thérapeutique.
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