RAD52 Functions in Homologous Recombination and Its Importance on Genomic Integrity Maintenance and Cancer Therapy

• Type: Another Publication in an International Scientific Journal
• Date: 2019

Authors

Nogueira, A (Author) Other; Fernandes, M (Author) Other; Catarino, R (Author) Other; Rui Medeiros (Author) ICBAS

Journal

Title: Cancers

Vol. 11

Final page: 1622

ISSN: 2072-6694

Publisher: MDPI

Indexing

ISI Web of Knowledge - 39 Citations

Scopus - 42 Citations

Other information

Authenticus ID: P-00R-81M

DOI: 10.3390/cancers11111622

Abstract (EN): 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.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 13