scholarly journals Induction of Tumor Cell Death through Targeting Tubulin and Evoking Dysregulation of Cell Cycle Regulatory Proteins by Multifunctional Cinnamaldehydes

PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e50125 ◽  
Author(s):  
Amrita A. Nagle ◽  
Fei-Fei Gan ◽  
Gavin Jones ◽  
Choon-Leng So ◽  
Geoffrey Wells ◽  
...  
2005 ◽  
Vol 12 (10) ◽  
pp. 1103-1115 ◽  
Author(s):  
Maureen Caligiuri ◽  
Frank Becker ◽  
Krishna Murthi ◽  
Faith Kaplan ◽  
Severine Dedier ◽  
...  

1990 ◽  
Vol 187 (2) ◽  
pp. 185-192 ◽  
Author(s):  
Jürgen van der Bosch ◽  
Stephan Rüller ◽  
Daniel Horn ◽  
Ralf Schumann ◽  
Max Schlaak

Toxicon ◽  
2010 ◽  
Vol 56 (7) ◽  
pp. 1145-1154 ◽  
Author(s):  
Ana Marisa Chudzinski-Tavassi ◽  
Paulo Luis De-Sá-Júnior ◽  
Simone Michaela Simons ◽  
Durvanei Augusto Maria ◽  
Janaina de Souza Ventura ◽  
...  

2019 ◽  
Vol 92 (1100) ◽  
pp. 20190283 ◽  
Author(s):  
Kristy Rieck ◽  
Kyle Bromma ◽  
Wonmo Sung ◽  
Aaron Bannister ◽  
Jan Schuemann ◽  
...  

Objective: The incorporation of high atomic number materials such as gold nanoparticles (GNPs) into tumor cells is being tested to enhance the local radiotherapy (RT) dose. It is also known that the radiosensitivity of tumor cells depends on the phase of their cell cycle. Triple combination of GNPs, phase of tumor cell population, and RT for improved outcomes in cancer treatment. Methods: We used a double-thymidine block method for synchronization of the tumor cell population. GNPs of diameters 17 and 46 nm were used to capture the size dependent effects. A radiation dose of 2 Gy with 6 MV linear accelerator was used to assess the efficacy of this proposed combined treatment. A triple negative breast cancer cell line, MDA-MB-231 was chosen as the model cell line. Monte Carlo (MC) calculations were done to predict the GNP-mediated cell death using the experimental GNP uptake data. Results: There was a 1.5- and 2- fold increase in uptake of 17 and 46 nm GNPs in the synchronized cell population, respectively. A radiation dose of 2 Gy with clinically relevant 6 MV photons resulted in a 62 and 38 % enhancement in cell death in the synchronized cell population with the incorporation of 17 and 46 nm GNPs, respectively. MC data supported the experimental data, but to a lesser extent. Conclusion: A triple combination of GNPs, cell cycle synchronization, and RT could pave the way to enhance the local radiation dose while minimizing side effects to the surrounding healthy tissue. Advances in knowledge: This is the first study to show that the combined use of GNPs, phase of tumor cell population, and RT could enhance tumor cell death.


Oncogene ◽  
2013 ◽  
Vol 33 (47) ◽  
pp. 5415-5423 ◽  
Author(s):  
A Newbold ◽  
J M Salmon ◽  
B P Martin ◽  
K Stanley ◽  
R W Johnstone

Cancers ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1280 ◽  
Author(s):  
Javier Vaquero ◽  
Florian Judée ◽  
Marie Vallette ◽  
Henri Decauchy ◽  
Ander Arbelaiz ◽  
...  

Through the last decade, cold atmospheric plasma (CAP) has emerged as an innovative therapeutic option for cancer treatment. Recently, we have set up a potentially safe atmospheric pressure plasma jet device that displays antitumoral properties in a preclinical model of cholangiocarcinoma (CCA), a rare and very aggressive cancer emerging from the biliary tree with few efficient treatments. In the present study, we aimed at deciphering the molecular mechanisms underlying the antitumor effects of CAP towards CCA in both an in vivo and in vitro context. In vivo, using subcutaneous xenografts into immunocompromised mice, CAP treatment of CCA induced DNA lesions and tumor cell apoptosis, as evaluated by 8-oxoguanine and cleaved caspase-3 immunohistochemistry, respectively. The analysis of the tumor microenvironment showed changes in markers related to macrophage polarization. In vitro, the incubation of CCA cells with CAP-treated culture media (i.e., plasma-activated media, PAM) led to a dose response decrease in cell survival. At molecular level, CAP treatment induced double-strand DNA breaks, followed by an increased phosphorylation and activation of the cell cycle master regulators CHK1 and p53, leading to cell cycle arrest and cell death by apoptosis. In conclusion, CAP is a novel therapeutic option to consider for CCA in the future.


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