RELATIONSHIP OF NUTRITIONAL FACTORS TO IN VITRO TUMOR CELL GROWTH AND CYTOTOXICITY PRODUCED BY CYTOSINE ARABINOSIDE

1977 ◽  
Vol 10 (2) ◽  
pp. 127-135
Author(s):  
Richard L. Momparler ◽  
Joel Goodman
Author(s):  
Lori Holle ◽  
Labri Hicks ◽  
Wendy Song ◽  
Eric Holle ◽  
Thomas Wagner ◽  
...  

2014 ◽  
Vol 38 (5) ◽  
pp. 608-612 ◽  
Author(s):  
Dai Chihara ◽  
Yoshitoyo Kagami ◽  
Harumi Kato ◽  
Noriaki Yoshida ◽  
Tohru Kiyono ◽  
...  

2018 ◽  
Vol 51 (4) ◽  
pp. 1969-1981 ◽  
Author(s):  
Xiangyu Zhu ◽  
Si-ping Ma ◽  
Dongxiang Yang ◽  
Yanlong Liu ◽  
Yong-peng Wang ◽  
...  

Background/Aims: Deregulation of microRNAs (miRNAs) has been associated with a variety of cancers, including colorectal cancer (CRC). Here, we investigated anomalous miR-142-3p expression and its possible functional consequences in primary CRC samples. Methods: The expression of miR-142-3p was measured by quantitative RT-PCR in 116 primary CRC tissues and adjacent non-tumor tissues. The effect of miR-142-3p up- or down-regulation in CRC-derived cells was evaluated in vitro by cell viability and colony formation assays and in vivo by growth assays in xenografted nude mice. Results: Using quantitative RT-PCR, we found that miR-142-3p was down-regulated in 78.4 % (91/116) of the primary CRC tissues tested when compared to the adjacent non-tumor tissues. We also found that the miR-142-3p mimic reduced in vitro cell viability and colony formation by inducing cell cycle arrest in CRC-derived cells, and inhibited in vivo tumor cell growth in xenografted nude mice. Inversely, we found that the miR-142-3p inhibitor increased the viability and colony forming capacity of CRC-derived cells and tumor cell growth in xenografted nude mice. In addition, we identified CDK4 as a potential target of miR-142-3p by predictions and dual-luciferase reporter assays. Concordantly, we found that miR-142-3p mimics and inhibitors could decrease and increase CDK4 protein levels in CRC-derived cells, respectively. Conclusion: From our results we conclude that miR-142-3p may act as a tumor suppressor in CRC and may serve as a tool for miRNA-based CRC therapy.


2012 ◽  
Vol 72 (20) ◽  
pp. 5374-5385 ◽  
Author(s):  
Marc S. Raab ◽  
Iris Breitkreutz ◽  
Simon Anderhub ◽  
Mads H. Rønnest ◽  
Blanka Leber ◽  
...  

2008 ◽  
Vol 183 (4) ◽  
pp. 737-749 ◽  
Author(s):  
Edwin Soto ◽  
Masahiro Yanagisawa ◽  
Laura A. Marlow ◽  
John A. Copland ◽  
Edith A. Perez ◽  
...  

p120 catenin regulates the activity of the Rho family guanosine triphosphatases (including RhoA and Rac1) in an adhesion-dependent manner. Through this action, p120 promotes a sessile cellular phenotype when associated with epithelial cadherin (E-cadherin) or a motile phenotype when associated with mesenchymal cadherins. In this study, we show that p120 also exerts significant and diametrically opposing effects on tumor cell growth depending on E-cadherin expression. Endogenous p120 acts to stabilize E-cadherin complexes and to actively promote the tumor-suppressive function of E-cadherin, potently inhibiting Ras activation. Upon E-cadherin loss during tumor progression, the negative regulation of Ras is relieved; under these conditions, endogenous p120 promotes transformed cell growth both in vitro and in vivo by activating a Rac1–mitogen-activated protein kinase signaling pathway normally activated by the adhesion of cells to the extracellular matrix. These data indicate that both E-cadherin and p120 are important regulators of tumor cell growth and imply roles for both proteins in chemoresistance and targeted therapeutics.


2016 ◽  
Author(s):  
Theo Sottero ◽  
Emily J. Girard ◽  
Colin Correnti ◽  
Mark R. Stroud ◽  
Brandon L. Kier ◽  
...  

1986 ◽  
Vol 39 (4) ◽  
pp. 447-456 ◽  
Author(s):  
Ronald Ross Watson ◽  
Satoru Moriguchi ◽  
Bart McRae ◽  
Lucia Tobin ◽  
J. Carter Mayberry ◽  
...  

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