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.

Abstract

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. However, 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.

• Authors: Takeshi Tomita, Katsuaki Ieguchi, Morichika Takita, Fujiko Tsukahara, Masayuki Yamada, Jean-Marc Egly, Yoshiro Maru
• Journal: Journal of biochemistry (J Biochem) Vol. 164 Issue 6 Pg. 415-426 (Dec 01 2018) ISSN: 1756-2651 [Electronic] England
• PMID: 30165670 (Publication Type: Comparative Study, Journal Article)

Chemical References

• Biomarkers
• C1D protein, human
• Co-Repressor Proteins
• DDIT3 protein, human
• DNA, Neoplasm
• Oxidants
• Pyrimidine Dimers
• pyrimidine-pyrimidone dimer
• Transcription Factor CHOP
• DNA
• Hydrogen Peroxide
• APEX1 protein, human
• DNA-(Apurinic or Apyrimidinic Site) Lyase

Topics

• Animals
• Biomarkers (metabolism)
• Cell Line, Tumor
• Cell Survival (drug effects, radiation effects)
• Co-Repressor Proteins (antagonists & inhibitors, genetics, metabolism)
• DNA (metabolism)
• DNA Damage
• DNA Repair (drug effects, radiation effects)
• DNA, Neoplasm (metabolism)
• DNA-(Apurinic or Apyrimidinic Site) Lyase (antagonists & inhibitors, chemistry, genetics, metabolism)
• Gene Expression Regulation, Enzymologic (drug effects, radiation effects)
• Gene Expression Regulation, Neoplastic (drug effects, radiation effects)
• Humans
• Hydrogen Peroxide (toxicity)
• Oxidants (toxicity)
• Oxidative Stress (drug effects, radiation effects)
• Pyrimidine Dimers (metabolism)
• RNA Interference
• Radiation Injuries, Experimental (enzymology, metabolism, pathology)
• Transcription Factor CHOP (agonists, antagonists & inhibitors, genetics, metabolism)