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.

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

https://www.ncbi.nlm.nih.gov/pubmed/30165670

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;: