Profiling of ribonucleotides and deoxyribonucleotides pools in response to DNA damage and repair induced by methyl methanesulfonate in cancer and normal cells
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Jian-Ru Guo1,*, Zheng Li1,*, Cai-Yun Wang1, Christopher Wai Kei Lam1, Qian-Qian Chen1, Wei-Jia Zhang2, Vincent Kam Wai Wong1, Mei-Cun Yao2 and Wei Zhang1
1State Key Laboratory of Quality Research in Chinese Medicines, Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology, Taipa, China
2School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou, China
*These authors have contributed equally to this work
Wei Zhang, email: email@example.com
Keywords: DNA damage; ribonucleotides; deoxyribonucleotides; perturbation; gene expression
Received: August 02, 2017 Accepted: September 03, 2017 Published: October 04, 2017
The absolute and relative pool sizes of deoxyribonucleotides (dRNs) are essential in DNA replication fidelity, DNA damage and repair. We found in this study that although DNA damage induced by methyl methanesulfonate (MMS) seemed similar in cancer (HepG2) and normal (LO2) cells, more extensive alterations in ribonucleotides (RNs) and dRNs pools occurred in HepG2 cells indicating that HepG2 cells were more vigilant to DNA damage. After 10 h repair, RNs pools were still severely perturbed in LO2 cells. Compared to LO2 cells, deoxyribonucleotide triphosphates (dNTPs) pools in HepG2 cells elevated by more folds which could facilitate more efficient DNA repair and improve survival probability following DNA damage, although this should definitely lead to higher mutation rates. DNA repair was more efficient in HepG2 cells at S phase and it partly came to an end while DNA repair was still uncompleted in LO2 cells outside S phase. In conclusion, our results demonstrated that HepG2 and LO2 cells presented many differences in nucleotide metabolism, cell cycle checkpoints and DNA repair pathways in response to DNA damage, which could be potential targets for cancer treatment.
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