Integrity of actin fibers and microtubules influences metastatic tumor cell adhesion

2004 ◽  
Vol 299 (1) ◽  
pp. 236-247 ◽  
Author(s):  
Timo Korb ◽  
Kerstin Schlüter ◽  
Andreas Enns ◽  
Hans-Ulrich Spiegel ◽  
Norbert Senninger ◽  
...  
2004 ◽  
Vol 8 (8) ◽  
pp. 1049-1060 ◽  
Author(s):  
A ENNS ◽  
P GASSMANN ◽  
K SCHLUTER ◽  
T KORB ◽  
H SPIEGEL ◽  
...  

2006 ◽  
Vol 169 (3) ◽  
pp. 1064-1073 ◽  
Author(s):  
Kerstin Schlüter ◽  
Peter Gassmann ◽  
Andreas Enns ◽  
Timo Korb ◽  
Andre Hemping-Bovenkerk ◽  
...  

2008 ◽  
Vol 14 (S2) ◽  
pp. 1512-1513
Author(s):  
MK ElZarrad ◽  
AB Al-Mehdi

Extended abstract of a paper presented at Microscopy and Microanalysis 2008 in Albuquerque, New Mexico, USA, August 3 – August 7, 2008


2019 ◽  
Vol 2 (4) ◽  
pp. e201900425 ◽  
Author(s):  
Yuko Matsumura ◽  
Yasuhiko Ito ◽  
Yoshihiro Mezawa ◽  
Kaidiliayi Sulidan ◽  
Yataro Daigo ◽  
...  

Emerging evidence supports the hypothesis that multicellular tumor clusters invade and seed metastasis. However, whether tumor-associated stroma induces epithelial–mesenchymal plasticity in tumor cell clusters, to promote invasion and metastasis, remains unknown. We demonstrate herein that carcinoma-associated fibroblasts (CAFs) frequently present in tumor stroma drive the formation of tumor cell clusters composed of two distinct cancer cell populations, one in a highly epithelial (E-cadherinhiZEB1lo/neg: Ehi) state and another in a hybrid epithelial/mesenchymal (E-cadherinloZEB1hi: E/M) state. The Ehi cells highly express oncogenic cell–cell adhesion molecules, such as carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5) and CEACAM6 that associate with E-cadherin, resulting in increased tumor cell cluster formation and metastatic seeding. The E/M cells also retain associations with Ehi cells, which follow the E/M cells leading to collective invasion. CAF-produced stromal cell-derived factor 1 and transforming growth factor-β confer the Ehi and E/M states as well as invasive and metastatic traits via Src activation in apposed human breast tumor cells. Taken together, these findings indicate that invasive and metastatic tumor cell clusters are induced by CAFs via epithelial–mesenchymal plasticity.


1997 ◽  
Vol 88 (1) ◽  
pp. 64-71 ◽  
Author(s):  
Yoshiko Abe ◽  
Tateki Tsutsui ◽  
Jie Mu ◽  
Atsushi Kosugi ◽  
Hideo Yagita ◽  
...  

1989 ◽  
Vol 61 (03) ◽  
pp. 485-489 ◽  
Author(s):  
Eva Bastida ◽  
Lourdes Almirall ◽  
Antonio Ordinas

SummaryBlood platelets are thought to be involved in certain aspects of malignant dissemination. To study the role of platelets in tumor cell adherence to vascular endothelium we performed studies under static and flow conditions, measuring tumor cell adhesion in the absence or presence of platelets. We used highly metastatic human adenocarcinoma cells of the lung, cultured human umbilical vein endothelial cells (ECs) and extracellular matrices (ECM) prepared from confluent EC monolayers. Our results indicated that under static conditions platelets do not significantly increase tumor cell adhesion to either intact ECs or to exposed ECM. Conversely, the studies performed under flow conditions using the flat chamber perfusion system indicated that the presence of 2 × 105 pl/μl in the perfusate significantly increased the number of tumor cells adhered to ECM, and that this effect was shear rate dependent. The maximal values of tumor cell adhesion were obtained, in presence of platelets, at a shear rate of 1,300 sec-1. Furthermore, our results with ASA-treated platelets suggest that the role of platelets in enhancing tumor cell adhesion to ECM is independent of the activation of the platelet cyclooxygenase pathway.


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