scholarly journals Abstract 3181: Nicotine promotes pre-metastatic niche formation in hormone receptor negative breast cancer through paracrine signaling in the tumor microenvironment

Author(s):  
Abhishek Tyagi ◽  
Sambad Sharma ◽  
Kerui Wu ◽  
Shih-Ying Wu ◽  
Dan Zhao ◽  
...  
2012 ◽  
Vol 90 (7) ◽  
pp. 803-815 ◽  
Author(s):  
Carmen Chak-Lui Wong ◽  
Huafeng Zhang ◽  
Daniele M. Gilkes ◽  
Jasper Chen ◽  
Hong Wei ◽  
...  

2020 ◽  
Author(s):  
Suzann Duan ◽  
Senny Nordmeier ◽  
Aidan E. Byrnes ◽  
Iain L. O. Buxton

AbstractMetastasis accounts for over 90% of cancer-related deaths. The mechanisms guiding this process remain unclear. Secreted nucleoside diphosphate kinase A and B (NDPK) support breast cancer metastasis. Proteomic evidence confirms their presence in breast cancer-derived extracellular vesicles (EVs). We investigated the role of EV-associated NDPK in modulating the host microenvironment in favor of pre-metastatic niche formation. We measured NDPK expression and activity in EVs isolated from triple-negative breast cancer (MDA-MB-231) and non-tumorigenic mammary epithelial (HME1) cells using flow cytometry, western blot, and ATP assay. We evaluated the effects of EV-associated NDPK on endothelial cell migration, vascular remodeling, and metastasis. We further assessed MDA-MB-231 EV induced-proteomic changes in support of pre-metastatic lung niche formation. NDPK-B expression and phosphotransferase activity were enriched in MDA-MB-231 EVs that promote vascular endothelial cell migration and disrupt monolayer integrity. MDA-MB-231 EV-treated mice demonstrate pulmonary vascular leakage and enhanced experimental lung metastasis, whereas treatment with an NDPK inhibitor or a P2Y1 purinoreceptor antagonist blunts these effects. We identified perturbations to the purinergic signaling pathway in experimental lungs, lending evidence to support a role for EV-associated NDPK-B in lung pre-metastatic niche formation and metastatic outgrowth.


2011 ◽  
Vol 108 (39) ◽  
pp. 16369-16374 ◽  
Author(s):  
C. C.-L. Wong ◽  
D. M. Gilkes ◽  
H. Zhang ◽  
J. Chen ◽  
H. Wei ◽  
...  

2015 ◽  
Vol 116 (12) ◽  
pp. 2730-2734 ◽  
Author(s):  
Atsushi Suetsugu ◽  
Masashi Momiyama ◽  
Yukihiko Hiroshima ◽  
Masahito Shimizu ◽  
Shigetoyo Saji ◽  
...  

2020 ◽  
Vol 21 (18) ◽  
pp. 6837 ◽  
Author(s):  
Issraa Shoucair ◽  
Fernanda Weber Mello ◽  
James Jabalee ◽  
Saeideh Maleki ◽  
Cathie Garnis

Extracellular vesicles (EVs) play a key role in the communication between cancer cells and stromal components of the tumor microenvironment (TME). In this context, cancer cell-derived EVs can regulate the activation of a CAF phenotype in TME cells, which can be mediated by several EV cargos (e.g., miRNA, proteins, mRNA and lncRNAs). On the other hand, CAF-derived EVs can mediate several processes during tumorigenesis, including tumor growth, invasion, metastasis, and therapy resistance. This review aimed to discuss the molecular aspects of EV-based cross-talk between CAFs and cancer cells during tumorigenesis, in addition to assessing the roles of EV cargo in therapy resistance and pre-metastatic niche formation.


Theranostics ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 1429-1445
Author(s):  
Xinxin Yuan ◽  
Niansong Qian ◽  
Shukuan Ling ◽  
Yuheng Li ◽  
Weijia Sun ◽  
...  

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