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Overcoming Therapy Resistance and Relapse in TNBC: Emerging Technologies to Target Breast Cancer-Associated
Farhana Mollah1, Pegah Varamini1,2
1Faculty of Medicine and Health, School of Pharmacy, University of Sydney, Sydney, NSW 2006, Australia.
Abstract:
Breast cancer is the most diagnosed cancer and is the leading cause of cancer mortality in women. Triple-negative breast cancer (TNBC) is an aggressive form of breast cancer. Often, TNBC is not effectively treated due to the lack of specificity of conventional therapies and results in relapse and metastasis. Breast cancer-associated fibroblasts (BCAFs) are the predominant cells that reside in the tumor microenvironment (TME) and regulate tumorigenesis, progression and metastasis, and therapy resistance. BCAFs secrete a wide range of factors, including growth factors, chemokines, and cytokines, some of which have been proved to lead to a poor prognosis and clinical outcomes. This TME component has been emerging as a promising target due to its crucial role in cancer progression and chemotherapy resistance. A number of therapeutic candidates are designed to effectively target BCAFs with a focus on their tumor-promoting properties and tumor immune response. This review explores various agents targeting BCAFs in TNBC, including small molecules, nucleic acid-based agents, antibodies, proteins, and finally, nanoparticles.
Insights
Triple-negative breast cancer (TNBC) is aggressive and hard to treat. Targeting breast cancer-associated fibroblasts (BCAFs) in the tumor microenvironment offers a promising therapeutic strategy for TNBC.
Area of Science:
- Oncology
- Cancer Biology
- Immunology
Background:
- Triple-negative breast cancer (TNBC) is an aggressive subtype with limited treatment options and high mortality.
- Breast cancer-associated fibroblasts (BCAFs) within the tumor microenvironment (TME) significantly contribute to TNBC progression, metastasis, and therapy resistance.
- BCAFs secrete factors that promote tumor growth and negatively impact patient prognosis.
Purpose of the Study:
- To review current therapeutic strategies targeting BCAFs in TNBC.
- To explore the role of BCAFs in TNBC pathogenesis and treatment resistance.
- To highlight emerging agents designed to inhibit BCAF-mediated tumor promotion.
Main Methods:
- Comprehensive literature review of studies investigating BCAFs in TNBC.
- Analysis of therapeutic agents targeting BCAFs, including small molecules, nucleic acids, antibodies, proteins, and nanoparticles.
- Evaluation of the impact of BCAF-targeting agents on tumor progression and immune response.
Main Results:
- BCAFs are critical regulators of TNBC, influencing tumorigenesis, metastasis, and resistance to conventional therapies.
- Various therapeutic modalities are being developed to target BCAFs, aiming to disrupt their pro-tumorigenic functions.
- Targeting BCAFs shows potential for improving treatment efficacy and patient outcomes in TNBC.
Conclusions:
- BCAFs represent a significant therapeutic target in TNBC due to their multifaceted roles in cancer progression.
- Targeting BCAFs offers a promising avenue for developing novel and more effective treatments for TNBC.
- Further research into BCAF-targeted therapies is crucial for advancing TNBC management.
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