Peroxiporins Are Induced upon Oxidative Stress Insult and Are Associated with Oxidative Stress Resistance in Colon Cancer Cell Lines
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 H<s...
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oai:doaj.org-article:efdf19850da74536b6e5ed0e23b02baa2021-11-25T16:29:55ZPeroxiporins Are Induced upon Oxidative Stress Insult and Are Associated with Oxidative Stress Resistance in Colon Cancer Cell Lines10.3390/antiox101118562076-3921https://doaj.org/article/efdf19850da74536b6e5ed0e23b02baa2021-11-01T00:00:00Zhttps://www.mdpi.com/2076-3921/10/11/1856https://doaj.org/toc/2076-3921Oxidative 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 H<sub>2</sub>O<sub>2</sub> 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 H<sub>2</sub>O<sub>2</sub>, cellular antioxidative status, and ROS intracellular accumulation after H<sub>2</sub>O<sub>2</sub> 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.Ana Čipak GašparovićLidija MilkovićClaudia RodriguesMonika MlinarićGraça SoveralMDPI AGarticleaquaporincolon cancer cell lineoxidative stressNRF2Therapeutics. PharmacologyRM1-950ENAntioxidants, Vol 10, Iss 1856, p 1856 (2021) |
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aquaporin colon cancer cell line oxidative stress NRF2 Therapeutics. Pharmacology RM1-950 |
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aquaporin colon cancer cell line oxidative stress NRF2 Therapeutics. Pharmacology RM1-950 Ana Čipak Gašparović Lidija Milković Claudia Rodrigues Monika Mlinarić Graça Soveral Peroxiporins Are Induced upon Oxidative Stress Insult and Are Associated with Oxidative Stress Resistance in Colon Cancer Cell Lines |
description |
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 H<sub>2</sub>O<sub>2</sub> 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 H<sub>2</sub>O<sub>2</sub>, cellular antioxidative status, and ROS intracellular accumulation after H<sub>2</sub>O<sub>2</sub> 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. |
format |
article |
author |
Ana Čipak Gašparović Lidija Milković Claudia Rodrigues Monika Mlinarić Graça Soveral |
author_facet |
Ana Čipak Gašparović Lidija Milković Claudia Rodrigues Monika Mlinarić Graça Soveral |
author_sort |
Ana Čipak Gašparović |
title |
Peroxiporins Are Induced upon Oxidative Stress Insult and Are Associated with Oxidative Stress Resistance in Colon Cancer Cell Lines |
title_short |
Peroxiporins Are Induced upon Oxidative Stress Insult and Are Associated with Oxidative Stress Resistance in Colon Cancer Cell Lines |
title_full |
Peroxiporins Are Induced upon Oxidative Stress Insult and Are Associated with Oxidative Stress Resistance in Colon Cancer Cell Lines |
title_fullStr |
Peroxiporins Are Induced upon Oxidative Stress Insult and Are Associated with Oxidative Stress Resistance in Colon Cancer Cell Lines |
title_full_unstemmed |
Peroxiporins Are Induced upon Oxidative Stress Insult and Are Associated with Oxidative Stress Resistance in Colon Cancer Cell Lines |
title_sort |
peroxiporins are induced upon oxidative stress insult and are associated with oxidative stress resistance in colon cancer cell lines |
publisher |
MDPI AG |
publishDate |
2021 |
url |
https://doaj.org/article/efdf19850da74536b6e5ed0e23b02baa |
work_keys_str_mv |
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