Ruthenium(II) complex containing cinnamic acid derivative inhibits cell cycle progression at G0/G1 and induces apoptosis in melanoma cells

2022 ◽  
Author(s):  
Amanda Negreti ◽  
Guilherme Álvaro Ferreira da Silva ◽  
Carolina G Pressete ◽  
Rafael Fonseca ◽  
Caio Cesar Candido ◽  
...  

Melanoma is a highly aggressive skin cancer with limited targeted therapy arsenal. The Ruthenium-based complexes have shown interesting pro-apoptotic effect on malignant tumor cell lines. In this study three Ruthenium(II)...

1995 ◽  
Vol 36 (5) ◽  
pp. 411-417 ◽  
Author(s):  
Christophe J. Bergeron ◽  
Hirak S. Basu ◽  
Laurence J. Marton ◽  
Dennis F. Deen ◽  
Malgorzata Pellarin ◽  
...  

1995 ◽  
Vol 36 (5) ◽  
pp. 411-417 ◽  
Author(s):  
Christophe J. Bergeron ◽  
Hirak S. Basu ◽  
Laurence J. Marton ◽  
Dennis F. Deen ◽  
Malgorzata Pellarin ◽  
...  

2010 ◽  
Vol 5 (1) ◽  
Author(s):  
Benjamin P Soule ◽  
Nicole L Simone ◽  
William G DeGraff ◽  
Rajani Choudhuri ◽  
John A Cook ◽  
...  

2005 ◽  
Vol 12 (10) ◽  
pp. 1103-1115 ◽  
Author(s):  
Maureen Caligiuri ◽  
Frank Becker ◽  
Krishna Murthi ◽  
Faith Kaplan ◽  
Severine Dedier ◽  
...  

Endocrine ◽  
2002 ◽  
Vol 17 (2) ◽  
pp. 119-128 ◽  
Author(s):  
Beverly C Delidow ◽  
Miranda Wang ◽  
Sonita V Bhamidipaty ◽  
Lynn D Black

Blood ◽  
2007 ◽  
Vol 110 (5) ◽  
pp. 1631-1638 ◽  
Author(s):  
Tint Lwin ◽  
Lori A. Hazlehurst ◽  
Sophie Dessureault ◽  
Raymond Lai ◽  
Wenlong Bai ◽  
...  

Abstract Mounting evidence suggests that dynamic interactions between a tumor and its microenvironment play a critical role in tumor development, cell-cycle progression, and response to therapy. In this study, we used mantle cell lymphoma (MCL) as a model to characterize the mechanisms by which stroma regulate cell-cycle progression. We demonstrated that adhesion of MCL and other non-Hodgkin lymphoma (NHL) cells to bone marrow stromal cells resulted in a reversible G1 arrest associated with elevated p27Kip1 and p21 (WAF1) proteins. The adhesion-mediated p27Kip1 and p21 increases were posttranslationally regulated via the down-regulation of Skp2, a subunit of SCFSkp2 ubiquitin ligase. Overexpression of Skp2 in MCL decreased p27Kip1, whereas inhibition of Skp2 by siRNA increased p27Kip1 and p21 levels. Furthermore, we found cell adhesion up-regulated Cdh1 (an activating subunit of anaphase-promoting complex [APC] ubiquitin ligase), and reduction of Cdh1 by siRNA induced Skp2 accumulation and hence p27Kip1 degradation, thus implicating Cdh1 as an upstream effector of the Skp2/p27Kip1 signaling pathway. Overall, this report, for the first time, demonstrates that cell-cell contact controls the tumor cell cycle via ubiquitin-proteasome proteolytic pathways in MCL and other NHLs. The understanding of this novel molecular pathway may prove valuable in designing new therapeutic approaches for modifying tumor cell growth and response to therapy.


Data in Brief ◽  
2020 ◽  
Vol 30 ◽  
pp. 105443 ◽  
Author(s):  
Gloria A. Santa-González ◽  
Edwin Patiño-González ◽  
Marcela Manrique-Moreno

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