A mechanisms of drug resistance in tumor endothelial cells

2020 ◽  
Vol 155 (5) ◽  
pp. 351-351
Author(s):  
Yui Kobayashi ◽  
Tatsuro Nakamura ◽  
Yusuke Miyazaki ◽  
Keisuke Omori ◽  
Koji Kobayashi ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Endothelial Cells ◽  
Tumor Endothelial Cells

scholarly journals miRNA-1246 in Extracellular Vesicles Secreted from Metastatic Tumor Induces Drug Resistance in Tumor Endothelial Cells

2020 ◽  
Author(s):  
Chisaho Torii ◽  
Nako Maishi ◽  
Taisuke Kawamoto ◽  
Masahiro Morimoto ◽  
Kosuke Akiyama ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Endothelial Cells ◽  
Induced Resistance ◽  
Extracellular Vesicles ◽  
Metastatic Tumor ◽  
Metastatic Tumors ◽  
Glycoprotein P ◽  
Tumor Endothelial Cells

Abstract Background: Tumor endothelial cells (TECs) reportedly exhibit altered phenotypes. We have demonstrated that TECs acquire drug resistance with the upregulation of p-glycoprotein (p-gp, ABCB1), contrary to traditional assumptions. Furthermore, p-gp expression was higher in TECs of highly metastatic tumors than in those of low metastatic tumors. However, the detailed mechanism of differential p-gp expression in TECs remains unclear. Methods: miRNA was identified in highly metastatic tumor extracellular vesicles (EVs) and the roles of miRNA in endothelial cell resistance were analyzed in vitro and in vivo. Results: In the present study, we found that treatment of highly metastatic tumor-conditioned medium induced resistance to 5-fluorouracil (5-FU) with interleukin-6 (IL-6) upregulation in endothelial cells (ECs). Among the soluble factors secreted from highly metastatic tumors, we focused on extracellular vesicles (EVs) and determined that miR-1246 was contained at a higher level in highly metastatic tumor EVs than in low metastatic tumor EVs. Furthermore, miR-1246 was transported via the EVs into ECs and induced IL-6 expression. Upregulated IL-6 induced resistance to 5-FU with STAT3 and Akt activation in ECs in an autocrine manner. Conclusions: These results suggested that highly metastatic tumors induce drug resistance in ECs by transporting miR-1246 through EVs.

scholarly journals Tumor endothelial cells with high aldehyde dehydrogenase activity show drug resistance

2017 ◽  
Vol 108 (11) ◽  
pp. 2195-2203 ◽  
Author(s):  
Kyoko Hida ◽  
Nako Maishi ◽  
Kosuke Akiyama ◽  
Hitomi Ohmura‐Kakutani ◽  
Chisaho Torii ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Endothelial Cells ◽  
Dehydrogenase Activity ◽  
Aldehyde Dehydrogenase ◽  
Tumor Endothelial Cells ◽  
Aldehyde Dehydrogenase Activity

scholarly journals Tumor Endothelial Cells Acquire Drug Resistance by MDR1 Up-Regulation via VEGF Signaling in Tumor Microenvironment

2012 ◽  
Vol 180 (3) ◽  
pp. 1283-1293 ◽  
Author(s):  
Kosuke Akiyama ◽  
Noritaka Ohga ◽  
Yasuhiro Hida ◽  
Taisuke Kawamoto ◽  
Yoshihiro Sadamoto ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Endothelial Cells ◽  
Tumor Microenvironment ◽  
Vegf Signaling ◽  
Tumor Endothelial Cells ◽  
Acquire Drug Resistance

scholarly journals miRNA-1246 in Extracellular Vesicles Secreted from Metastatic Tumor Induces Drug Resistance in Tumor Endothelial Cells

2020 ◽  
Author(s):  
Chisaho Torii ◽  
Nako Maishi ◽  
Taisuke Kawamoto ◽  
Masahiro Morimoto ◽  
Kosuke Akiyama ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Endothelial Cells ◽  
Extracellular Vesicles ◽  
Metastatic Tumor ◽  
Tumor Endothelial Cells

Abstract The authors have withdrawn this preprint due to author disagreement.

scholarly journals miRNA-1246 in extracellular vesicles secreted from metastatic tumor induces drug resistance in tumor endothelial cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Chisaho Torii ◽  
Nako Maishi ◽  
Taisuke Kawamoto ◽  
Masahiro Morimoto ◽  
Kosuke Akiyama ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Endothelial Cells ◽  
Induced Resistance ◽  
Extracellular Vesicles ◽  
Metastatic Tumor ◽  
Metastatic Tumors ◽  
Glycoprotein P ◽  
Tumor Endothelial Cells

AbstractTumor endothelial cells (TECs) reportedly exhibit altered phenotypes. We have demonstrated that TECs acquire drug resistance with the upregulation of P-glycoprotein (P-gp, ABCB1), contrary to traditional assumptions. Furthermore, P-gp expression was higher in TECs of highly metastatic tumors than in those of low metastatic tumors. However, the detailed mechanism of differential P-gp expression in TECs remains unclear. miRNA was identified in highly metastatic tumor extracellular vesicles (EVs) and the roles of miRNA in endothelial cell resistance were analyzed in vitro and in vivo. In the present study, we found that treatment of highly metastatic tumor-conditioned medium induced resistance to 5-fluorouracil (5-FU) with interleukin-6 (IL-6) upregulation in endothelial cells (ECs). Among the soluble factors secreted from highly metastatic tumors, we focused on EVs and determined that miR-1246 was contained at a higher level in highly metastatic tumor EVs than in low metastatic tumor EVs. Furthermore, miR-1246 was transported via the EVs into ECs and induced IL-6 expression. Upregulated IL-6 induced resistance to 5-FU with STAT3 and Akt activation in ECs in an autocrine manner. These results suggested that highly metastatic tumors induce drug resistance in ECs by transporting miR-1246 through EVs.

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