Resumen
DNA is prone to damages, which would result in genetic disorders and enhance risk of tumorigenesis. Hence, understanding the molecular mechanisms of DNA damage and repair will provide deep insights into tumorigenesis, carcinogenesis as well as the corresponding treatments. Aiming at investigating potential long noncoding RNAs (lncRNAs) response against DNA damage, we performed a comprehensive transcriptomic analysis based on RNA sequencing data of the liver tissue from Rattus norvegicus, in which DNA damage was induced using aflatoxin B1, ifosfamide and N-nitrosodimethylamine. Through our analyses, numerous novel lncRNAs are identified for the first time, and differential network analysis discloses lncRNA-mediated regulatory networks related to DNA-damage response. The result shows that these DNA-damage-inducing chemicals might disrupt many lncRNA-mediated interactions involved in diverse biological processes and pathways, for example, immune function and cell adhesion. In contrast, the host might also activate a few RNA interactions in response to DNA damage, involving response to drug and regulation of cell cycle.
| Idioma original | English |
|---|---|
| Páginas (desde-hasta) | 23216-23231 |
| Número de páginas | 16 |
| Publicación | Journal of Cellular Physiology |
| Volumen | 234 |
| N.º | 12 |
| DOI | |
| Estado | Published - dic 2019 |
Nota bibliográfica
Publisher Copyright:© 2019 Wiley Periodicals, Inc.
Financiación
We thank Xiao Qiang Sun of the Sun Yat‐sen University for helpful discussions and comments on the manuscript, particularly in network analysis. This study was supported by the University of Macau through Research Grants MYRG2018‐00071‐FHS, EF005/FHS‐ZXH/2018/GSTIC, and FHS‐CRDA‐029‐002‐2017. We thank Xiao Qiang Sun of the Sun Yat-sen University for helpful discussions and comments on the manuscript, particularly in network analysis. This study was supported by the University of Macau through Research Grants MYRG2018-00071-FHS, EF005/FHS-ZXH/2018/GSTIC, and FHS-CRDA-029-002-2017.
| Financiadores | Número del financiador |
|---|---|
| Xiao Qiang Sun of the Sun Yat-sen University | |
| Universidade de Macau | EF005/FHS‐ZXH/2018/GSTIC, FHS‐CRDA‐029‐002‐2017 |
| Universidade de Macau |
ASJC Scopus subject areas
- Physiology
- Clinical Biochemistry
- Cell Biology