RAD52 Functions in Homologous Recombination and Its Importance on Genomic Integrity Maintenance and Cancer Therapy
Autor: | Raquel Catarino, Rui Medeiros, Mara Fernandes, Augusto Nogueira |
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Jazyk: | angličtina |
Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Cancer Research Cell cycle checkpoint DNA damage DNA repair RAD52 genetic processes rad52 homologous recombination Review Biology medicine.disease_cause lcsh:RC254-282 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine fungi lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cell biology dna damage response enzymes and coenzymes (carbohydrates) 030104 developmental biology Oncology chemistry 030220 oncology & carcinogenesis cancer therapy dna damage Carcinogenesis Homologous recombination carcinogenesis DNA RAD52 Gene |
Zdroj: | Cancers, Vol 11, Iss 11, p 1622 (2019) Cancers |
ISSN: | 2072-6694 |
Popis: | Genomes are continually subjected to DNA damage whether they are induced from intrinsic physiological processes or extrinsic agents. Double-stranded breaks (DSBs) are the most injurious type of DNA damage, being induced by ionizing radiation (IR) and cytotoxic agents used in cancer treatment. The failure to repair DSBs can result in aberrant chromosomal abnormalities which lead to cancer development. An intricate network of DNA damage signaling pathways is usually activated to eliminate these damages and to restore genomic stability. These signaling pathways include the activation of cell cycle checkpoints, DNA repair mechanisms, and apoptosis induction, also known as DNA damage response (DDR)-mechanisms. Remarkably, the homologous recombination (HR) is the major DSBs repairing pathway, in which RAD52 gene has a crucial repairing role by promoting the annealing of complementary single-stranded DNA and by stimulating RAD51 recombinase activity. Evidence suggests that variations in RAD52 expression can influence HR activity and, subsequently, influence the predisposition and treatment efficacy of cancer. In this review, we present several reports in which the down or upregulation of RAD52 seems to be associated with different carcinogenic processes. In addition, we discuss RAD52 inhibition in DDR-defective cancers as a possible target to improve cancer therapy efficacy. |
Databáze: | OpenAIRE |
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