scholarly journals Transient receptor potential melastatin-related 7 channel is overexpressed in human pancreatic ductal adenocarcinomas and regulates human pancreatic cancer cell migration

2012 ◽  
Vol 131 (6) ◽  
pp. E851-E861 ◽  
Author(s):  
Pierre Rybarczyk ◽  
Mathieu Gautier ◽  
Frédéric Hague ◽  
Isabelle Dhennin-Duthille ◽  
Denis Chatelain ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Migration ◽  
Transient Receptor Potential ◽  
Pancreatic Cancer Cell ◽  
Receptor Potential ◽  
Human Pancreatic Cancer ◽  
Cancer Cell Migration ◽  
Human Pancreatic Cancer Cell ◽  
Transient Receptor Potential Melastatin ◽  
Transient Receptor

scholarly journals The Transient Receptor Potential Melastatin 7 Channel Regulates Pancreatic Cancer Cell Invasion through the Hsp90α/uPA/MMP2 pathway

Neoplasia ◽  
2017 ◽  
Vol 19 (4) ◽  
pp. 288-300 ◽  
Author(s):  
Pierre Rybarczyk ◽  
Alison Vanlaeys ◽  
Bertrand Brassart ◽  
Isabelle Dhennin-Duthille ◽  
Denis Chatelain ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Transient Receptor Potential ◽  
Pancreatic Cancer Cell ◽  
Receptor Potential ◽  
Cancer Cell Invasion ◽  
Transient Receptor Potential Melastatin ◽  
Transient Receptor

The Bioflavonoid Baicalein Inhibits Human Pancreatic Cancer Cell Migration

2013 ◽  
Vol 179 (2) ◽  
pp. 310 ◽  
Author(s):  
G.W. Donald ◽  
M. Chen ◽  
A. Moro ◽  
H. Pham ◽  
K.M. Hertzer ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Human Pancreatic Cancer ◽  
Cancer Cell Migration ◽  
Human Pancreatic Cancer Cell

scholarly journals Transient Receptor Potential Melastatin 4 (TRPM4) Contributes to High Salt Diet-Mediated Early-Stage Endothelial Injury

2017 ◽  
Vol 41 (2) ◽  
pp. 835-848 ◽  
Author(s):  
Xiao-Qing Ding ◽  
Tao Ban ◽  
Zeng-Yan Liu ◽  
Jie Lou ◽  
Liang-Liang Tang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Cell Migration ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
High Salt Diet ◽  
Salt Diet ◽  
Transient Receptor Potential Melastatin ◽  
Intracellular Ros ◽  
Transient Receptor

Background/Aims: The present study investigated whether the transient receptor potential melastatin 4 (TRPM4) channel plays a role in high salt diet (HSD)-induced endothelial injuries. Methods: Western blotting and immunofluorescence were used to examine TRPM4 expression in the mesenteric endothelium of Dahl salt-sensitive (SS) rats fed a HSD. The MTT, TUNEL, and transwell assays were used to evaluate the cell viability, cell apoptosis, and cell migration, respectively, of human umbilical vein endothelial cells (HUVECs). Enzyme-linked immunosorbent assays were used to determine the concentrations of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion protein 1 (VCAM-1), and E-selectin. Carboxy-H2DCFDA, a membrane-permeable reactive oxygen species (ROS)-sensitive fluorescent probe, was used to detect intracellular ROS levels. Results: TRPM4 was mainly expressed near the plasma membrane of mesenteric artery endothelial cells, and its expression level increased in SS hypertensive rats fed a HSD. Its protein expression was significantly upregulated upon treatment with exogenous hydrogen peroxide (H2O2) and aldosterone in cultured HUVECs. Cell viability decreased upon treatment with both agents in a concentration-dependent manner, which could be partially reversed by 9-phenanthrol, a specific TRPM4 inhibitor. Exogenous H2O2 induced apoptosis, enhanced cell migration, and increased the release of adhesion molecules, including ICAM-1, VCAM-1, and E-selectin, all of which were significantly attenuated upon treatment with 9-phenanthrol. Aldosterone and H2O2 induced the accumulation of intracellular ROS, which was significantly inhibited by 9-phenanthrol, suggesting that oxidative stress is one of the mechanisms underlying aldosterone-induced endothelial injury. Conclusions: Given the fact that oxidative stress and high levels of circulating aldosterone are present in hypertensive patients, we suggest that the upregulation of TRPM4 in the vascular endothelium may be involved in endothelial injuries caused by these stimuli.

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