C1D is not directly involved in the repair of UV-damaged DNA but protects cells from oxidative stress by regulating gene expressions in human cell lines.
Fiche publication
Date publication
août 2018
Journal
Journal of biochemistry
Auteurs
Membres identifiés du Cancéropôle Est :
Dr EGLY Jean-Marc
Tous les auteurs :
Tomita T, Ieguchi K, Takita M, Tsukahara F, Yamada M, Egly JM, Maru Y
Lien Pubmed
Résumé
A small nuclear protein, C1D, has roles in various cellular processes, transcription regulation, genome stability surveillance, DNA repair, and RNA processing, all of which are required to maintain the host life cycles. In the previous report, C1D directly interacts with XPB, a component of the nucleotide excision repair complex, and C1D knockdown reduced cell survival of 27-1 cells, CHO derivative cells, after UV irradiation. To find out the role of C1D in UV damaged cells, we used human cell lines with siRNA or shRNA to knockdown C1D. C1D knockdown reduced cell survival rates of LU99 and 786-O after UV irradiation, although C1D knockdown did not affect the efficiency of the nucleotide excision repair. Immunostaining data support that C1D is not directly involved in the DNA repair process in UV damaged cells. On the other hand, H2O2 treatment reduced cell viability in LU99 and 786-O cells. We also found that C1D knockdown upregulated DDIT3 expression in LU99 cells and downregulated APEX1 in 786-O cells, suggesting that C1D functions as a co-repressor/activator. The data accounts for the reduction of cell survival rates upon UV irradiation.
Mots clés
Animals, Biomarkers, metabolism, Cell Line, Tumor, Cell Survival, drug effects, Co-Repressor Proteins, antagonists & inhibitors, DNA, metabolism, DNA Damage, DNA Repair, drug effects, DNA, Neoplasm, metabolism, DNA-(Apurinic or Apyrimidinic Site) Lyase, antagonists & inhibitors, Gene Expression Regulation, Enzymologic, drug effects, Gene Expression Regulation, Neoplastic, drug effects, Humans, Hydrogen Peroxide, toxicity, Oxidants, toxicity, Oxidative Stress, drug effects, Pyrimidine Dimers, metabolism, RNA Interference, Radiation Injuries, Experimental, enzymology, Transcription Factor CHOP, agonists
Référence
J. Biochem.. 2018 Aug 27;: