scholarly journals PAR-type thrombin receptors in renal carcinoma cells: PAR1-mediated EGFR activation promotes cell migration

2006 ◽  
Author(s):  
Sebastian Bergmann ◽  
Kerstin Junker ◽  
Peter Henklein ◽  
Morley Hollenberg ◽  
Utz Settmacher ◽  
...  
Keyword(s):  
Cell Migration ◽  
Renal Carcinoma ◽  
Carcinoma Cells ◽  
Thrombin Receptors ◽  
Egfr Activation ◽  
Renal Carcinoma Cells

scholarly journals Alpha-Mangostin Suppresses the Metastasis of Human Renal Carcinoma Cells by Targeting MEK/ERK Expression and MMP-9 Transcription Activity

2017 ◽  
Vol 44 (4) ◽  
pp. 1460-1470 ◽  
Author(s):  
Chien-Min Chen ◽  
Shu-Ching Hsieh ◽  
Chia-Liang Lin ◽  
Yu-Syun Lin ◽  
Jen-Pi Tsai ◽  
...  
Keyword(s):  
Cell Migration ◽  
Renal Carcinoma ◽  
Carcinoma Cells ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Cell Migration And Invasion ◽  
Human Renal Carcinoma ◽  
Renal Carcinoma Cells

Background/Aims: α-mangostin has anti-carcinogenic effects against several cancers. We investigated the molecular mechanism of this compound on the metastasis of human renal carcinoma cells. Methods: Cell viability was measured using the MTT assay, and cell cycle distribution using flow cytometry. A Matrigel-based assay was used to measure in vitro cell migration and invasion. MAPK-related proteins and matrix metalloproteinase (MMP)-9 and MMP-2 expression were measured by western blotting, and MMP2/-9 activities were determined by gelatin zymography. RT-qPCR and a luciferase assay were used to examine the transcriptional activity of MMP-9. Results: α-mangostin inhibited the migration and invasion of RCC cells in a dose-dependent manner, but had no evident cytotoxic effects. Treatment of 786-O cells with α-mangostin inhibited activation of MEK and ERK. Treatment with a specific MEK inhibitor (U0126) enhanced the inhibitory effects of α-mangostin on cell migration and invasion, and the phosphorylation of ERK and MEK. Moreover, α-mangostin inhibited the expression of the MMP-9 mRNA levels as well as the activity of MMP-9 promoter, and these suppressive effects were further enhanced by U0126. Conclusions: Our results suggest that α-mangostin suppresses cell migration and invasion via MEK/ERK/MMP9 pathway, and might be a promising anti-metastatic agent against human renal cell carcinoma.

The Indolylcoumarin COUFIN Exhibits Potent Activity Against Renal Carcinoma Cells without Affecting Hematopoietic System

2014 ◽  
Vol 14 (6) ◽  
pp. 862-871 ◽  
Author(s):  
Pierre Champelovier ◽  
Pascale Barbier ◽  
Etienne Daras ◽  
Soazig Douillard ◽  
Bertrand Toussaint ◽  
...  
Keyword(s):  
Renal Carcinoma ◽  
Carcinoma Cells ◽  
Hematopoietic System ◽  
Renal Carcinoma Cells

scholarly journals Cooperative Blockade of CK2 and ATM Kinases Drives Apoptosis in VHL-Deficient Renal Carcinoma Cells through ROS Overproduction

Cancers ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 576
Author(s):  
Sofia Giacosa ◽  
Catherine Pillet ◽  
Irinka Séraudie ◽  
Laurent Guyon ◽  
Yann Wallez ◽  
...  
Keyword(s):  
High Throughput Screening ◽  
Renal Carcinoma ◽  
Kinase Inhibitors ◽  
Ex Vivo ◽  
Cancer Therapeutics ◽  
Carcinoma Cells ◽  
Wild Type ◽  
Cell Renal Cell Carcinoma ◽  
Von Hippel Lindau ◽  
Renal Carcinoma Cells

Kinase-targeted agents demonstrate antitumor activity in advanced metastatic clear cell renal cell carcinoma (ccRCC), which remains largely incurable. Integration of genomic approaches through small-molecules and genetically based high-throughput screening holds the promise of improved discovery of candidate targets for cancer therapy. The 786-O cell line represents a model for most ccRCC that have a loss of functional pVHL (von Hippel-Lindau). A multiplexed assay was used to study the cellular fitness of a panel of engineered ccRCC isogenic 786-O VHL− cell lines in response to a collection of targeted cancer therapeutics including kinase inhibitors, allowing the interrogation of over 2880 drug–gene pairs. Among diverse patterns of drug sensitivities, investigation of the mechanistic effect of one selected drug combination on tumor spheroids and ex vivo renal tumor slice cultures showed that VHL-defective ccRCC cells were more vulnerable to the combined inhibition of the CK2 and ATM kinases than wild-type VHL cells. Importantly, we found that HIF-2α acts as a key mediator that potentiates the response to combined CK2/ATM inhibition by triggering ROS-dependent apoptosis. Importantly, our findings reveal a selective killing of VHL-deficient renal carcinoma cells and provide a rationale for a mechanism-based use of combined CK2/ATM inhibitors for improved patient care in metastatic VHL-ccRCC.

The autophagy sensor ITPR1 protects renal carcinoma cells from NK-mediated killing

Autophagy ◽  
2015 ◽  
pp. 00-00 ◽  
Author(s):  
Yosra Messai ◽  
Muhammad Zaeem Noman ◽  
Bassam Janji ◽  
Meriem Hasmim ◽  
Bernard Escudier ◽  
...  
Keyword(s):  
Renal Carcinoma ◽  
Carcinoma Cells ◽  
Renal Carcinoma Cells
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