Identification of a chemotherapeutic lead molecule for the potential disruption of the FAM72A-UNG2 interaction to interfere with genome stability, centromere formation, and genome editingopen access
- Authors
- Renganathan, Senthil; Pramanik, Subrata; Ekambaram, Rajasekaran; Kutzner, Arne; Kim, Pok-Son; Heese, Klaus
- Issue Date
- Nov-2021
- Publisher
- MDPI
- Keywords
- Cell cycle; Centromere; DNA repair; Proliferation
- Citation
- CANCERS, v.13, no.22, pp.1 - 19
- Indexed
- SCIE
SCOPUS
- Journal Title
- CANCERS
- Volume
- 13
- Number
- 22
- Start Page
- 1
- End Page
- 19
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/140418
- DOI
- 10.3390/cancers13225870
- Abstract
- Family with sequence similarity 72 A (FAM72A) is a pivotal mitosis-promoting factor that is highly expressed in various types of cancer. FAM72A interacts with the uracil-DNA glycosylase UNG2 to prevent mutagenesis by eliminating uracil from DNA molecules through cleaving the Nglycosylic bond and initiating the base excision repair pathway, thus maintaining genome integrity. In the present study, we determined a specific FAM72A-UNG2 heterodimer protein interaction using molecular docking and dynamics. In addition, through in silico screening, we identified withaferin B as a molecule that can specifically prevent the FAM72A-UNG2 interaction by blocking its cell signaling pathways. Our results provide an excellent basis for possible therapeutic approaches in the clinical treatment of cancer.
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Collections - 서울 의생명공학전문대학원 > 서울 의생명공학전문대학원 > 1. Journal Articles
- 서울 공과대학 > 서울 정보시스템학과 > 1. Journal Articles
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