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Ganoderma lucidum and oxidative DNA damage: the role cellular antioxidant system
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SYSNO ASEP 0475624 Document Type C - Proceedings Paper (int. conf.) R&D Document Type O - Ostatní Title Ganoderma lucidum and oxidative DNA damage: the role cellular antioxidant system Author(s) Opattová, Alena (UEM-P)
Kozics, K. (SK)
Čumová, Andrea (UEM-P)
Slíva, D. (CZ)
Vodenková, S. (US)
Vodička, Pavel (UEM-P) RIDSource Title Cellular signalling and cancer therapy. - Cavtat : EMBO Conference, 2016 Pages s. 172-172 Number of pages 1 s. Action Cellular signalling and cancer therapy Event date 27.05.2016 - 31.05.2016 VEvent location Cavtat Country HR - Croatia Language eng - English Country HR - Croatia Keywords colorectal cancer ; natural compound ; oxidative DNA damage ; DNA repair ; colorectal cell lines Subject RIV EE - Microbiology, Virology R&D Projects LH13061 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) GA15-14789S GA ČR - Czech Science Foundation (CSF) NV15-27580A GA MZd - Ministry of Health (MZ) Institutional support UEM-P - RVO:68378041 Annotation Reactive oxygen species (ROS) are a group of highly reactive molecules tightly controlled by cellular antioxidant system. Disturbance in the prooxidation–antioxidation homeostasis can lead to ROS accumulation and consequently to DNA damage, as well as apoptosis. Many natural compounds such as Ganoderma lucidum (GLC) possess anticancer activities with the generation of ROS. Because the cancer cells are most sensitive to oxidative DNA damage as non-cancerous cells, oxidative damage is a potential target to enhance the activity of anticancer treatment by natural compounds which may lead to selective cancer cell death.
The aim of our study was to define effect of GLC extracts on cellular antioxidant system, oxidative DNA damage in colorectal cell lines (HTC116, HCT116-/-, HT29). Our results showed that 24 hrs GLC treatment (0,5mg/ml) inhibits activity of SOD1 (25%, p<0.01) in HCT116 as well as enzymatic activity of GpX (20%, p<0.01), followed by abnormal reactive oxygen species accumulation. Moreover, GLC significantly decreased a level of nuclear respiratory factor1 (NRF1), transcription factor critical for expression of antioxidant response dependent genes. The specific oxidative DNA damage increased (x%, p<0.05) after GLC treatment (0.5mg/ml, p<0.05), whereas the specific DNA repair process was inhibited. Finally, this led to decreased HCT116 survival (25%, p<0.05).
Our results clearly suggest that GLC extract strongly decrease activity of cellular antioxidant system and lead oxidative DNA damage and cell death in colorectal cancer cell lines. This indicates that natural compounds with prooxidant activity are potential target for selective improvement of anti-cancer treatment.
Workplace Institute of Experimental Medicine Contact Lenka Koželská, lenka.kozelska@iem.cas.cz, Tel.: 241 062 218, 296 442 218 Year of Publishing 2017
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