Sirt3 regulates the level of mitochondrial DNA repair activity through deacetylation of NEIL1, NEIL2, OGG1, MUTYH, APE1 and LIG3 in colorectal cancer

• Authors: Jacek Kabziński , Anna Walczak , Michał Mik , Ireneusz Majsterek

Abstracts

EN

Colorectal cancer (CRC) is one of the most common malignant tumors. One of the factors increasing the risk of its occurrence may be the reduced efficiency of repairing DNA damage, both nuclear and mitochondrial. The main mechanism for repairing oxidative damage is the BER system (in mitochondria mtBER), whose key proteins NEIL1, NEIL2, OGG1, MUTYH, APE1 and LIG3 obtain full efficiency only at the appropriate level of acetylation. Sirtuin 3 is a key protein for mitochondrial homeostasis, regulating a number of metabolic processes related mainly to the control of the level of reactive oxygen species. Because Sirt3 possesses acetylase activity, it can modulate the level of activity of mtBER proteins by their deacetylation. The conducted study showed that the tested proteins NEIL1, NEIL2, OGG1, MUTYH, APE1 and LIG3 are the substrate for the enzymatic deacetylation activity of Sirt3, which may lead to modulation of the risk of CRC, and in cancer cells may be a potential therapeutic target enhancing the action of cytostatic drugs.

Keywords

EN

cancer; colorectal cancer; DNA damage/repair; genetics; proteins

• Publisher: Index Copernicus International
• Journal: Polish Journal of Surgery
• Year: 2020
• Volume: 92(1)
• Pages: 1-4

Dates

published

2019-11-04

Contributors

author

Jacek Kabziński

author

Anna Walczak

author

Michał Mik

author

Ireneusz Majsterek

Identifiers

DOI

10.5604/01.3001.0013.5539