Calcium-channel-blockers exhibit divergent regulation of cancer extravasation through the mechanical properties of cancer cells and underlying vascular endothelial cells

2021 ◽  
Author(s):  
S. R. Vaibavi ◽  
Manoj Sivasubramaniapandian ◽  
Rahul Vaippully ◽  
Privita Edwina ◽  
Basudev Roy ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Endothelial Cells ◽  
Calcium Channel ◽  
Cancer Cells ◽  
Calcium Channel Blockers ◽  
Vascular Endothelial Cells ◽  
Channel Blockers ◽  
Vascular Endothelial

YAP Overexpression in Breast Cancer Cells Promotes Angiogenesis Through Activating Yap Signaling in Vascular Endothelial Cells

2020 ◽  
Author(s):  
Yu Yan ◽  
Qiang Song ◽  
Li Yao ◽  
Liang Zhao ◽  
Hui Cai
Keyword(s):  
Breast Cancer ◽  
Endothelial Cells ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Tumor Angiogenesis ◽  
Breast Cancer Cells ◽  
Vascular Endothelial Cells ◽  
Tissue Growth ◽  
Vascular Endothelial ◽  
Potential Marker

Abstract Background:The YAP signaling pathway is altered and implicated as oncogenic in human mammary cancers.However, roles of YAP signaling that regulate the breast tumor angiogenesis have remained elusive. Tumor angiogenesis is coordinated by the activation of both cancer cells and vascular endothelial cells. Whether the YAP signalingpathway can regulate the intercellular interaction between cancer cells and endothelial cellsis essentially unknown.Results: We showed here that conditioned media from YAP overexpressed breast cancer cells (CM-YAP+) could promote angiogenesis, accompanied byincreased tube formation, migration, and proliferation of human umbilical vein endothelial cells (HUVECs). Down regulation of YAP in HUVECs reversed CM-YAP+ induced angiogenesis.CM-YAP+ time-dependently activated YAP inHUVECs by dephosphorylating YAP and increasing nuclear translocation.We also identified that both G13-RhoA and PI3K/Akt signaling pathway were necessary for CM-YAP+ induced activation of YAP.Besides, connective tissue growth factor (CTGF) and angiopoietin-2 (ANG-2)actedas down-stream of YAP in HUVECs to promote angiogenesis.In addition, subcutaneous tumors nude mice model demonstrated that tumors overexpressed YAP revealed moreneovascularization in vivo.Conclusions: YAP-YAP interaction between breastcancer cells and endothelial cellscould promote tumor angiogenesis, supporting that YAP is a potential marker and target fordeveloping novel therapeutic strategies against breast cancer.

Elastase Activity Enhances the Adhesion of Neutrophil and Cancer Cells to Vascular Endothelial Cells

2000 ◽  
Vol 94 (2) ◽  
pp. 153-158 ◽  
Author(s):  
Fumiaki Nozawa ◽  
Masahiko Hirota ◽  
Akihiro Okabe ◽  
Muneyuki Shibata ◽  
Takeshi Iwamura ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cancer Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Elastase Activity

Growth inhibition of human cancer cells in vitro by T-type calcium channel blockers

2006 ◽  
Vol 16 (19) ◽  
pp. 5014-5017 ◽  
Author(s):  
Jae Yeol Lee ◽  
Seong Jun Park ◽  
Sung Jun Park ◽  
Min Joo Lee ◽  
Hyewhon Rhim ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Calcium Channel ◽  
Cancer Cells ◽  
Calcium Channel Blockers ◽  
Human Cancer ◽  
Channel Blockers ◽  
Human Cancer Cells

Inhibitory Effect of Calcium Channel Blockers on Growth of Pancreatic Cancer Cells

Pancreas ◽  
1994 ◽  
Vol 9 (2) ◽  
pp. 193-202 ◽  
Author(s):  
Kazuo Sato ◽  
Jin Ishizuka ◽  
Cary W. Cooper ◽  
Dai H. Chung ◽  
Takashi Tsuchiya ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Calcium Channel ◽  
Cancer Cells ◽  
Calcium Channel Blockers ◽  
Inhibitory Effect ◽  
Channel Blockers ◽  
Pancreatic Cancer Cells

scholarly journals The ATF6-EGF Pathway Mediates the Awakening of Slow-Cycling Chemoresistant Cells and Tumor Recurrence by Stimulating Tumor Angiogenesis

Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1772
Author(s):  
Jaebeom Cho ◽  
Hye-Young Min ◽  
Honglan Pei ◽  
Xuan Wei ◽  
Jeong Yeon Sim ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cancer Cells ◽  
Tumor Recurrence ◽  
Vascular Endothelial Cells ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Epidermal Growth ◽  
Slow Cycling

Slow-cycling cancer cells (SCCs) with a quiescence-like phenotype are believed to perpetrate cancer relapse and progression. However, the mechanisms that mediate SCC-derived tumor recurrence are poorly understood. Here, we investigated the mechanisms underlying cancer recurrence after chemotherapy, focusing on the interplay between SCCs and the tumor microenvironment. We established a preclinical model of SCCs by exposing non-small-cell lung cancer (NSCLC) cells to either the proliferation-dependent dye carboxyfluorescein diacetate succinimidyl ester (CFSE) or chemotherapeutic drugs. An RNA sequencing analysis revealed that the established SCCs exhibited the upregulation of a group of genes, especially epidermal growth factor (EGF). Increases in the number of vascular endothelial growth factor receptor (VEGFR)-positive vascular endothelial cells and epidermal growth factor receptor (EGFR) activation were found in NSCLC cell line- and patient-derived xenograft tumors that progressed upon chemotherapy. EGFR tyrosine kinase inhibitors effectively suppressed the migration and tube formation of vascular endothelial cells. Furthermore, activating transcription factor 6 (ATF6) induced the upregulation of EGF, and its antagonism effectively suppressed these SCC-mediated events and inhibited tumor recurrence after chemotherapy. These results suggest that the ATF6-EGF signaling axis in SCCs functions to trigger the angiogenesis switch in residual tumors after chemotherapy and is thus a driving force for the switch from SCCs to actively cycling cancer cells, leading to tumor recurrence.

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