Abstract
Chlamydia trachomatis infections have been associated with ovarian cancer by several epidemiological studies. Here, we show that C. trachomatis-infected primary human ovarian epithelial cells display elevated oxidative DNA damage. Base excision repair, an important cellular mechanism to repair oxidative DNA lesions, was impaired in infected primary ovarian and in several other types of cells. Polymerase β was downregulated in infected cells associated with upregulation of microRNA-499a (miR-499a). Stabilising polymerase β by inhibiting miR-499a significantly improved repair. Moreover, downregulation of tumour suppressor p53 also resulted in attenuated repair in these cells. Thus, our data show that downregulation of polymerase β by direct inhibition through miR-499a and downregulation of p53 debilitate the host-cell base excision repair during C. trachomatis infection.
Original language | English |
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Pages (from-to) | e12986 |
Journal | Cellular Microbiology |
Volume | 21 |
Issue number | 4 |
DOIs | |
Publication status | Published - Apr 2019 |
Externally published | Yes |
Keywords*
- Chlamydia Infections/metabolism
- Chlamydia trachomatis/pathogenicity
- DNA Damage/genetics
- DNA Repair/genetics
- Down-Regulation
- Epithelial Cells/metabolism
- Female
- Humans
- Immunoblotting
- Ovary/cytology
- Real-Time Polymerase Chain Reaction
Field of Science*
- 3.1 Basic medicine
- 1.6 Biological sciences
- 3.3 Health sciences
Publication Type*
- 1.1. Scientific article indexed in Web of Science and/or Scopus database