E2F1 promotes progression of bladder cancer by modulating RAD54L involved in homologous recombination repair

Cited 21 time in scopus
Metadata Downloads
Title
E2F1 promotes progression of bladder cancer by modulating RAD54L involved in homologous recombination repair
Author(s)
J Y Mun; Seung Woo Baek; W Y Park; W T Kim; Seon-Kyu Kim; Y G Roh; M S Jeong; G E Yang; J H Lee; J W Chung; Y H Choi; In-Sun Chu; S H Leem
Bibliographic Citation
International Journal of Molecular Sciences, vol. 21, no. 23, pp. 9025-9025
Publication Year
2020
Abstract
DNA repair defects are important factors in cancer development. High DNA repair activity can affect cancer progression and chemoresistance. DNA double-strand breaks in cancer cells caused by anticancer agents can be restored by non-homologous end joining (NHEJ) and homologous recombination repair (HRR). Our previous study has identified E2F1 as a key gene in bladder cancer progression. In this study, DNA repair genes related to E2F1 were analyzed, and RAD54L involved in HRR was identified. In gene expression analysis of bladder cancer patients, the survival of patients with high RAD54L expression was shorter with cancer progression than in patients with low RAD54L expression. This study also revealed that E2F1 directly binds to the promoter region of RAD54L and regulates the transcription of RAD54L related to the HRR pathway. This study also confirmed that DNA breaks are repaired by RAD54L induced by E2F1 in bladder cancer cells treated with MMC. In summary, RAD54L was identified as a new target directly regulated by E2F1. Our results suggest that, E2F1 and RAD54L could be used as diagnostic markers for bladder cancer progression and represent potential therapeutic targets.
Keyword
bladder cancerhomologous recombination repairE2F1RAD54Lprognostic biomarkers
ISSN
1661-6596
Publisher
MDPI
DOI
http://dx.doi.org/10.3390/ijms21239025
Type
Article
Appears in Collections:
Aging Convergence Research Center > 1. Journal Articles
Division of Biomedical Research > Metabolic Regulation Research Center > 1. Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.