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Epigenetic Regulation of Autophagy in Breast Cancer: Implications for Biomarker Discovery and Personalized Therapy
1Department of Precision Medicine, University of Campania "Luigi Vanvitelli,", Naples, Italy.
Background:
Breast cancer remains one of the most common and lethal malignancies among women. Despite advanced targeted therapies and precision medicine, therapeutic resistance continues to undermine durable clinical responses. Increasing evidence links epigenetic dysregulation and autophagy as central contributors to breast cancer progression, therapy resistance, and metabolic changes. Histone modifications, non-coding RNAs, and DNA methylation dynamically regulate autophagy-related genes (ATGs), while autophagy itself co-regulates the epigenetic landscape under chemotherapeutic stress. This two-way interplay determines tumor cell fate, influencing sensitivity to chemotherapy, endocrine therapy, and targeted agents.
Aims:
This article reviews recent studies on epigenetic mechanisms modulating autophagy and their impact on resistance pathways in breast cancer. Furthermore, this article highlighted the emerging role of epigenetic-autophagy as a biomarker for early detection, disease monitoring, and predicting therapeutic response.
Conclusion:
Finally, the review outlined new therapeutic methods that combine epigenetic modulators and autophagy inhibitors with particular attention to AI-driven drug discovery and precision oncology. Collectively, this review emphasizes the potential of targeting epigenetic-autophagy crosstalk to overcome therapy resistance and improve patient outcomes.
Insights
Epigenetic changes and autophagy are key to breast cancer resistance. Targeting their interaction may improve treatment effectiveness and patient outcomes in precision oncology.
Area of Science:
- Oncology
- Epigenetics
- Molecular Biology
Background:
- Breast cancer is a leading cause of death in women, with therapeutic resistance limiting treatment efficacy.
- Epigenetic dysregulation and autophagy are increasingly recognized as critical factors in breast cancer progression and resistance.
- The interplay between epigenetic modifications (histone modifications, non-coding RNAs, DNA methylation) and autophagy regulates genes involved in cancer cell fate and drug sensitivity.
Purpose of the Study:
- To review recent research on how epigenetic mechanisms influence autophagy in breast cancer.
- To explore the role of the epigenetic-autophagy axis in mediating resistance to various cancer therapies.
- To highlight the potential of epigenetic-autophagy interactions as biomarkers for early detection and treatment response prediction.
Main Methods:
- Literature review of recent studies on epigenetic regulation of autophagy in breast cancer.
- Analysis of the impact of epigenetic-autophagy crosstalk on therapeutic resistance pathways.
- Exploration of emerging biomarkers and therapeutic strategies targeting this interplay.
Main Results:
- Epigenetic modifications dynamically regulate autophagy-related genes, influencing breast cancer cell survival and drug response.
- Autophagy, in turn, can modulate the epigenetic landscape, particularly under stress conditions like chemotherapy.
- This bidirectional crosstalk is a significant determinant of sensitivity to chemotherapy, endocrine therapy, and targeted agents.
Conclusions:
- Targeting the epigenetic-autophagy crosstalk presents a promising strategy to overcome therapeutic resistance in breast cancer.
- Combination therapies involving epigenetic modulators and autophagy inhibitors show potential for improved patient outcomes.
- AI-driven drug discovery and precision oncology approaches can accelerate the development of novel treatments for this complex interplay.
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