scholarly journals Both Farnesylated and Geranylgeranylated RhoB Inhibit Malignant Transformation and Suppress Human Tumor Growth in Nude Mice

2000 ◽  
Vol 275 (24) ◽  
pp. 17974-17978 ◽  
Author(s):  
Zhi Chen ◽  
Jiazhi Sun ◽  
Anne Pradines ◽  
Gilles Favre ◽  
Jalila Adnane ◽  
...  
2011 ◽  
Vol 302 (2) ◽  
pp. 119-127 ◽  
Author(s):  
Fujia Lv ◽  
Yuhe Qiu ◽  
Yaxi Zhang ◽  
Shilian Liu ◽  
Juan Shi ◽  
...  

APOPTOSIS ◽  
2009 ◽  
Vol 14 (10) ◽  
pp. 1190-1203 ◽  
Author(s):  
Magali Brabant ◽  
Ludwig Baux ◽  
Richard Casimir ◽  
Jean Paul Briand ◽  
Olivier Chaloin ◽  
...  

2006 ◽  
Vol 175 (4S) ◽  
pp. 263-263
Author(s):  
Christoph Kündig ◽  
Sylvain M. Cloutier ◽  
Steve Aellen ◽  
Loyse M. Felber ◽  
Jair R. Chagas ◽  
...  

2019 ◽  
Vol 65 (5) ◽  
pp. 760-765
Author(s):  
Margarita Tyndyk ◽  
Irina Popovich ◽  
A. Malek ◽  
R. Samsonov ◽  
N. Germanov ◽  
...  

The paper presents the results of the research on the antitumor activity of a new drug - atomic clusters of silver (ACS), the colloidal solution of nanostructured silver bisilicate Ag6Si2O7 with particles size of 1-2 nm in deionized water. In vitro studies to evaluate the effect of various ACS concentrations in human tumor cells cultures (breast cancer, colon carcinoma and prostate cancer) were conducted. The highest antitumor activity of ACS was observed in dilutions from 2.7 mg/l to 5.1 mg/l, resulting in the death of tumor cells in all studied cell cultures. In vivo experiments on transplanted Ehrlich carcinoma model in mice consuming 0.75 mg/kg ACS with drinking water revealed significant inhibition of tumor growth since the 14th day of experiment (maximally by 52% on the 28th day, p < 0.05) in comparison with control. Subcutaneous injections of 2.5 mg/kg ACS inhibited Ehrlich's tumor growth on the 7th and 10th days of the experiment (p < 0.05) as compared to control.


Blood ◽  
2016 ◽  
Vol 127 (13) ◽  
pp. 1676-1686 ◽  
Author(s):  
Zubin Zhang ◽  
Jiefei Tong ◽  
Xiaowen Tang ◽  
Jiaxiang Juan ◽  
Biyin Cao ◽  
...  

Key Points HERC4 is the first identified ubiquitin ligase that mediates c-Maf ubiquitination and degradation. HERC4 suppresses MM cell proliferation and delays MM tumor growth.


Metabolism ◽  
2001 ◽  
Vol 50 (10) ◽  
pp. 1213-1219 ◽  
Author(s):  
N. Nara-Ashizawa ◽  
T. Tsukada ◽  
K. Maruyama ◽  
Y. Akiyama ◽  
N. Kajimura ◽  
...  

1995 ◽  
Vol 15 (8) ◽  
pp. 4249-4259 ◽  
Author(s):  
A M Yahanda ◽  
J M Bruner ◽  
L A Donehower ◽  
R S Morrison

Loss or mutation of p53 is thought to be an early event in the malignant transformation of many human astrocytic tumors. To better understand the role of p53 in their growth and transformation, we developed a model employing cultured neonatal astrocytes derived from mice deficient in one (p53 +/-) or both (p53 -/-) p53 alleles, comparing them with wild-type (p53 +/+) cells. Studies of in vitro and in vivo growth and transformation were performed, and flow cytometry and karyotyping were used to correlate changes in growth with genomic instability. Early-passage (EP) p53 -/- astrocytes achieved higher saturation densities and had more rapid growth than EP p53 +/- and +/+ cells. The EP p53 -/- cells were not transformed, as they were unable to grow in serum-free medium or in nude mice. With continued passaging, p53 -/- cells exhibited a multistep progression to a transformed phenotype. Late-passage p53 -/- cells achieved saturation densities 50 times higher than those of p53 +/+ cells and formed large, well-vascularized tumors in nude mice. p53 +/- astrocytes exhibited early loss of the remaining wild-type p53 allele and then evolved in a manner phenotypically similar to p53 -/- astrocytes. In marked contrast, astrocytes retaining both wild-type p53 alleles never exhibited a transformed phenotype and usually senesced after 7 to 10 passages. Dramatic alterations in ploidy and karyotype occurred and were restricted to cells deficient in wild-type p53 following repeated passaging. The results of these studies suggest that loss of wild-type p53 function promotes genomic instability, accelerated growth, and malignant transformation in astrocytes.


Sign in / Sign up

Export Citation Format

Share Document