scholarly journals Enhanced Oxidative Stress Resistance through Activation of a Zinc Deficiency Transcription Factor in Brachypodium distachyon

2014 ◽  
Vol 166 (3) ◽  
pp. 1492-1505 ◽  
Author(s):  
K. M. Glover-Cutter ◽  
S. Alderman ◽  
J. E. Dombrowski ◽  
R. C. Martin
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Zinc Deficiency ◽  
Stress Resistance ◽  
Brachypodium Distachyon ◽  
Oxidative Stress Resistance

scholarly journals A new regulator in the crossroads of oxidative stress resistance and virulence in Candida glabrata: The transcription factor CgTog1

Virulence ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 1522-1538
Author(s):  
Pedro Pais ◽  
Susana Vagueiro ◽  
Dalila Mil-Homens ◽  
Andreia I. Pimenta ◽  
Romeu Viana ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Stress Resistance ◽  
Candida Glabrata ◽  
Oxidative Stress Resistance

scholarly journals Role of rgsA in Oxidative Stress Resistance in Pseudomonas aeruginosa

2021 ◽  
Author(s):  
Shuyi Hou ◽  
Jiaqin Zhang ◽  
Xiaobo Ma ◽  
Qiang Hong ◽  
Lili Fang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pseudomonas Aeruginosa ◽  
Stress Resistance ◽  
Oxidative Stress Resistance

scholarly journals Peroxiporins Are Induced Upon Oxidative Stress Insult and Are Associated with Oxidative Stress Resistance in Colon Cancer Cell Lines

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1856
Author(s):  
Ana Čipak Gašparović ◽  
Lidija Milković ◽  
Claudia Rodrigues ◽  
Monika Mlinarić ◽  
Graça Soveral
Keyword(s):  
Oxidative Stress ◽  
Colon Cancer ◽  
Transcription Factor ◽  
Cell Lines ◽  
Stress Resistance ◽  
Therapy Resistance ◽  
Colon Cancer Cell ◽  
Colon Cancer Cell Lines ◽  
Intracellular Ros ◽  
Ht 29

Oxidative stress can induce genetic instability and change cellular processes, resulting in colorectal cancer. Additionally, adaptation of oxidative defense causes therapy resistance, a major obstacle in successful cancer treatment. Peroxiporins are aquaporin membrane channels that facilitate H2O2 membrane permeation, crucial for regulating cell proliferation and antioxidative defense. Here, we investigated four colon cancer cell lines (Caco-2, HT-29, SW620, and HCT 116) for their sensitivity to H2O2, cellular antioxidative status, and ROS intracellular accumulation after H2O2 treatment. The expression of peroxiporins AQP1, AQP3, and AQP5 and levels of NRF2, the antioxidant transcription factor, and PPARγ, a transcription factor that regulates lipid metabolism, were evaluated before and after oxidative insult. Of the four tested cell lines, HT-29 was the most resistant and showed the highest expression of all tested peroxiporins and the lowest levels of intracellular ROS, without differences in GSH levels, catalase activity, nor NF2 and PPARγ levels. Caco-2 shows high expression of AQP3 and similar resistance as HT-29. These results imply that oxidative stress resistance can be obtained by several mechanisms other than the antioxidant defense system. Regulation of intracellular ROS through modulation of peroxiporin expression may represent an additional strategy to target the therapy resistance of cancer cells.

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