Extracellular vesicle-mediated transport: Reprogramming a tumor microenvironment conducive with breast cancer progression and metastasis
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. Ex...
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2022
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oai:doaj.org-article:8af156e49ea04ffb8c31f27bca39bbac2021-11-28T04:29:53ZExtracellular vesicle-mediated transport: Reprogramming a tumor microenvironment conducive with breast cancer progression and metastasis1936-523310.1016/j.tranon.2021.101286https://doaj.org/article/8af156e49ea04ffb8c31f27bca39bbac2022-01-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S1936523321002771https://doaj.org/toc/1936-5233Breast 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.Dara BrenaMing-Bo HuangVincent BondElsevierarticleMetastatic breast cancerExtracellular vesicleTumor microenvironmentPre-metastatic nichePrecision medicineNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENTranslational Oncology, Vol 15, Iss 1, Pp 101286- (2022) |
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DOAJ |
collection |
DOAJ |
language |
EN |
topic |
Metastatic breast cancer Extracellular vesicle Tumor microenvironment Pre-metastatic niche Precision medicine Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 |
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Metastatic breast cancer Extracellular vesicle Tumor microenvironment Pre-metastatic niche Precision medicine Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Dara Brena Ming-Bo Huang Vincent Bond Extracellular vesicle-mediated transport: Reprogramming a tumor microenvironment conducive with breast cancer progression and metastasis |
description |
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. |
format |
article |
author |
Dara Brena Ming-Bo Huang Vincent Bond |
author_facet |
Dara Brena Ming-Bo Huang Vincent Bond |
author_sort |
Dara Brena |
title |
Extracellular vesicle-mediated transport: Reprogramming a tumor microenvironment conducive with breast cancer progression and metastasis |
title_short |
Extracellular vesicle-mediated transport: Reprogramming a tumor microenvironment conducive with breast cancer progression and metastasis |
title_full |
Extracellular vesicle-mediated transport: Reprogramming a tumor microenvironment conducive with breast cancer progression and metastasis |
title_fullStr |
Extracellular vesicle-mediated transport: Reprogramming a tumor microenvironment conducive with breast cancer progression and metastasis |
title_full_unstemmed |
Extracellular vesicle-mediated transport: Reprogramming a tumor microenvironment conducive with breast cancer progression and metastasis |
title_sort |
extracellular vesicle-mediated transport: reprogramming a tumor microenvironment conducive with breast cancer progression and metastasis |
publisher |
Elsevier |
publishDate |
2022 |
url |
https://doaj.org/article/8af156e49ea04ffb8c31f27bca39bbac |
work_keys_str_mv |
AT darabrena extracellularvesiclemediatedtransportreprogrammingatumormicroenvironmentconducivewithbreastcancerprogressionandmetastasis AT mingbohuang extracellularvesiclemediatedtransportreprogrammingatumormicroenvironmentconducivewithbreastcancerprogressionandmetastasis AT vincentbond extracellularvesiclemediatedtransportreprogrammingatumormicroenvironmentconducivewithbreastcancerprogressionandmetastasis |
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1718408389974818816 |