scholarly journals Transcription Factor CUTL1 Is a Negative Regulator of Drug Resistance in Gastric Cancer

2012 ◽  
Vol 288 (6) ◽  
pp. 4135-4147 ◽  
Author(s):  
Tingting Li ◽  
Honghong Wang ◽  
Yimin Sun ◽  
Lina Zhao ◽  
Yi Gang ◽  
...  
2001 ◽  
Vol 120 (5) ◽  
pp. A31-A31
Author(s):  
H KATAOKA ◽  
T JOH ◽  
T OHSHIMA ◽  
Y ITOH ◽  
K SENOO ◽  
...  

2012 ◽  
Vol 23 ◽  
pp. iv37-iv38
Author(s):  
Juliana Oliveira ◽  
Aledson Felipe ◽  
Paula Chang ◽  
Tiago da Silva ◽  
Célia Pimenta ◽  
...  

2017 ◽  
Vol 16 (7) ◽  
pp. 1537 ◽  
Author(s):  
Lian Xiaowen ◽  
Li Kesheng ◽  
Du Huifen ◽  
Li Xingwen ◽  
Cui Yan ◽  
...  

2019 ◽  
Vol 20 (15) ◽  
pp. 3736 ◽  
Author(s):  
Sabino Russi ◽  
Henu Kumar Verma ◽  
Simona Laurino ◽  
Pellegrino Mazzone ◽  
Giovanni Storto ◽  
...  

Despite the significant recent advances in clinical practice, gastric cancer (GC) represents a leading cause of cancer-related deaths in the world. In fact, occurrence of chemo-resistance still remains a daunting hindrance to effectiveness of the current approach to GC therapy. There is accumulating evidence that a plethora of cellular and molecular factors is implicated in drug-induced phenotypical switching of GC cells. Among them, epithelial-mesenchymal transition (EMT), autophagy, drug detoxification, DNA damage response and drug target alterations, have been reported as major determinants. Intriguingly, resistant GC phenotype may be the result of GC cell-induced tumor microenvironment (TME) remodeling, which is currently emerging as a key player in promoting drug resistance and overcoming cytotoxic effects of drugs. In this review, we discuss the possible mechanisms of drug resistance and their involvement in determining current GC therapies failure.


2001 ◽  
Vol 75 (13) ◽  
pp. 5796-5811 ◽  
Author(s):  
Tina Nilsson ◽  
Henrik Zetterberg ◽  
Yuyan Camilla Wang ◽  
Lars Rymo

ABSTRACT The identification of the cellular factors that control the transcription regulatory activity of the Epstein-Barr virus C promoter (Cp) is fundamental to the understanding of the molecular mechanisms that control virus latent gene expression. Using transient transfection of reporter plasmids in group I phenotype B-lymphoid cells, we have previously shown that the −248 to −55 region (−248/−55 region) of Cp contains elements that are essential fororiPI-EBNA1-dependent as well asoriPI-EBNA1-independent activation of the promoter. We now establish the importance of this region by a detailed mutational analysis of reporter plasmids carrying Cp regulatory sequences together with or without oriPI. The reporter plasmids were transfected into group I phenotype Rael cells and group III phenotype cbc-Rael cells, and the Cp activity measured was correlated with the binding of candidate transcription factors in electrophoretic mobility shift assays and further assessed in cotransfection experiments. We show that the NF-Y transcription factor interacts with the previously identified CCAAT box in the −71/−63 Cp region (M. T. Puglielli, M. Woisetschlaeger, and S. H. Speck, J. Virol. 70:5758–5768, 1996). We also show that members of the C/EBP transcription factor family interact with a C/EBP consensus sequence in the −119/−112 region of Cp and that this interaction is important for promoter activity. A central finding is the identification of a GC-rich sequence in the −99/−91 Cp region that is essential fororiPI-EBNA1-independent as well asoriPI-EBNA1-dependent activity of the promoter. This region contains overlapping binding sites for Sp1 and Egr-1, and our results suggest that Sp1 is a positive and Egr-1 is a negative regulator of Cp activity. Furthermore, we demonstrate that a reporter plasmid that in addition to oriPI contains only the −111/+76 region of Cp still retains the ability to be activated by EBNA1.


The Analyst ◽  
2018 ◽  
Vol 143 (1) ◽  
pp. 164-174 ◽  
Author(s):  
Yong Zhang ◽  
Ludi Jin ◽  
Jingjing Xu ◽  
Yuezhou Yu ◽  
Lin Shen ◽  
...  

Drug resistance and heterogeneous characteristics of human gastric carcinoma cells (BGC823) under the treatment of paclitaxel (PTX) were investigated using single-cell Raman spectroscopy (RS).


2009 ◽  
Vol 69 (8) ◽  
pp. 3501-3509 ◽  
Author(s):  
Qiang Li ◽  
Nu Zhang ◽  
Zhiliang Jia ◽  
Xiangdong Le ◽  
Bingbing Dai ◽  
...  

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