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Extracellular vesicle-mediated transport: Reprogramming a tumor microenvironment conducive with breast cancer
Dara Brena1, Ming-Bo Huang1, Vincent Bond1
1Department of Microbiology, Biochemistry, and Immunology, Morehouse School of Medicine, Atlanta, GA 30310, United States.
Abstract:
Breast cancer metastatic progression to critical secondary sites is the second leading cause of cancer-related mortality in women. While existing therapies are highly effective in combating primary tumors, metastatic disease is generally deemed incurable with a median survival of only 2, 3 years. Extensive efforts have focused on identifying metastatic contributory targets for therapeutic antagonism and prevention to improve patient survivability. Excessive breast cancer release of extracellular vesicles (EVs), whose contents stimulate a metastatic phenotype, represents a promising target. Complex breast cancer intercellular communication networks are based on EV transport and transference of molecular information is in bulk resulting in complete reprogramming events within recipient cells. Other breast cancer cells can acquire aggressive phenotypes, endothelial cells can be induced to undergo tubule formation, and immune cells can be neutralized. Recent advancements continue to implicate the critical role EVs play in cultivating a tumor microenvironment tailored to cancer proliferation, metastasis, immune evasion, and conference of drug resistance. This literature review serves to frame the role of EV transport in breast cancer progression and metastasis. The following five sections will be addressed: (1) Intercellular communication in developing a tumor microenvironment & pre-metastatic niche. (2) Induction of the epithelial-to-mesenchymal transition (EMT). (3). Immune suppression & evasion. (4) Transmission of drug resistance mechanisms. (5) Precision medicine: clinical applications of EVs.
Insights
Breast cancer extracellular vesicles (EVs) drive metastasis by reprogramming recipient cells. Targeting EV communication offers a novel strategy to combat metastatic breast cancer and improve patient survival.
Area of Science:
- Oncology
- Cell Biology
- Molecular Biology
Background:
- Metastatic breast cancer progression is a leading cause of cancer mortality.
- Current therapies are ineffective against metastatic disease, necessitating new therapeutic targets.
- Extracellular vesicles (EVs) released by breast cancer cells play a critical role in metastasis.
Purpose of the Study:
- To review the role of EV transport in breast cancer progression and metastasis.
- To highlight EVs' contribution to the tumor microenvironment, epithelial-to-mesenchymal transition, immune suppression, and drug resistance.
- To discuss the clinical applications of EVs in precision medicine for breast cancer.
Main Methods:
- Literature review of scientific articles on extracellular vesicles and breast cancer metastasis.
- Analysis of EV-mediated intercellular communication mechanisms.
- Synthesis of current research on EVs in tumor microenvironment modulation, EMT induction, immune evasion, and drug resistance transmission.
Main Results:
- EVs facilitate intercellular communication, reprogramming recipient cells to promote metastasis.
- EVs contribute to the formation of a pre-metastatic niche, epithelial-to-mesenchymal transition (EMT), immune suppression, and drug resistance.
- EVs are implicated in cultivating a tumor microenvironment conducive to cancer proliferation and immune evasion.
Conclusions:
- EVs are central mediators of breast cancer metastasis and therapeutic resistance.
- Targeting EV-mediated communication represents a promising therapeutic strategy.
- Further research into EVs holds potential for developing novel precision medicine approaches for breast cancer treatment.
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