Extracellular vesicle-mediated transport: Reprogramming a tumor microenvironment conducive with breast cancer progression and metastasis.
Extracellular vesicle-mediated transport: Reprogramming a tumor microenvironment conducive with breast cancer progression and metastasis.
复制标题
DOI:
10.1016/j.tranon.2021.101286
复制
发表时间:
2022-01
影响因子:
5
通讯作者:
Bond V
中科院分区:
文献类型:
--
作者:
Brena D;Huang MB;Bond V
Extracellular vesicles’ (EVs) role in breast tumor microenvironment and pre-metastatic niche development. Breast cancer EV-mediated transmission of pro-metastatic and drug-resistant phenotypes. Precision medicine with EVs as biomarkers and delivery vehicles for drug and anticancer genetic material. 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.
登录
查看更多内容
影响因子:
64.5
作者:
Boelens MC;Wu TJ;Nabet BY;Xu B;Qiu Y;Yoon T;Azzam DJ;Twyman-Saint Victor C;Wiemann BZ;Ishwaran H;Ter Brugge PJ;Jonkers J;Slingerland J;Minn AJ
通讯作者:
Minn AJ
影响因子:
3.7
作者:
Chen WX;Liu XM;Lv MM;Chen L;Zhao JH;Zhong SL;Ji MH;Hu Q;Luo Z;Wu JZ;Tang JH
通讯作者:
Tang JH
影响因子:
11.2
作者:
Ashiru O;Boutet P;Fernández-Messina L;Agüera-González S;Skepper JN;Valés-Gómez M;Reyburn HT
通讯作者:
Reyburn HT
DOI:
10.1007/s10555-016-9639-8
发表时间:
2016-12
期刊:
Cancer metastasis reviews
影响因子:
--
作者:
Chin AR;Wang SE
通讯作者:
Wang SE
影响因子:
7.3
作者:
Barros FM;Carneiro F;Machado JC;Melo SA
通讯作者:
Melo SA