Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 23, Issue 4, Pages -Publisher
MDPI
DOI: 10.3390/ijms23042328
Keywords
BoHV-1; beta-catenin; 53BP1; gamma H2AX; DNA damage
Funding
- Chinese National Science Foundation [31972655, 31772743.]
- High-level Talents Research Start-up Project of Hebei University [521100221087]
- Priority Academic Program Development (PAPD) of Jiangsu Higher Education Institutions
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The study demonstrates that BoHV-1 infection disrupts DNA damage repair mediated by 53BP1 and suggests that β-catenin plays a role in restricting both virus replication and DNA damage in A549 cells.
Oncolytic bovine herpesvirus type 1 (BoHV-1) infection induces DNA damage in human lung adenocarcinoma cell line A549. However, the underlying mechanisms are not fully understood. We found that BoHV-1 infection decreased the steady-state protein levels of p53-binding protein 1 (53BP1), which plays a central role in dictating DNA damage repair and maintaining genomic stability. Furthermore, BoHV-1 impaired the formation of 53BP1 foci, suggesting that BoHV-1 inhibits 53BP1-mediated DNA damage repair. Interestingly, BoHV-1 infection redistributed intracellular beta-catenin, and iCRT14 (5-[[2,5-Dimethyl-1-(3-pyridinyl)-1H-pyrrol-3-yl]methylene]-3-phenyl-2,4-thiazolidinedione), a beta-catenin-specific inhibitor, enhanced certain viral protein expression, such as the envelope glycoproteins gC and gD, and enhanced virus infection-induced DNA damage. Therefore, for the first time, we provide evidence showing that BoHV-1 infection disrupts 53BP1-mediated DNA damage repair and suggest beta-catenin as a potential host factor restricting both virus replication and DNA damage in A549 cells.
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