Interplay between base excision repair protein XRCC1 and ALDH2 predicts overall survival in lung and liver cancer patients

Cell Oncol (Dordr). 2018 Oct;41(5):527-539. doi: 10.1007/s13402-018-0390-8. Epub 2018 Aug 7.

Abstract

Background: To deliver efficacious personalised cancer treatment, it is essential to characterise the cellular metabolism as well as the genetic stability of individual tumours. In this study, we describe a new axis between DNA repair and detoxification of aldehyde derivatives with important implications for patient prognosis and treatment.

Methods: Western blot and qPCR analyses were performed in relevant non-transformed and cancer cell lines from lung and liver tissue origin in combination with bioinformatics data mining of The Cancer Genome Atlas database from lung and hepatocellular cancer patients.

Results: Using both biochemical and bioinformatics approaches, we revealed an association between the levels of expression of the aldehyde detoxifying enzyme aldehyde dehydrogenase 2 (ALDH2) and the key DNA base excision repair protein XRCC1. Across cancer types, we found that if one of the corresponding genes exhibits a low expression level, the level of the other gene is increased. Surprisingly, we found that low ALDH2 expression levels associated with high XRCC1 expression levels are indicative for a poor overall survival, particularly in lung and liver cancer patients. In addition, we found that Mithramycin A, a XRCC1 expression inhibitor, efficiently kills cancer cells expressing low levels of ALDH2.

Conclusions: Our data suggest that lung and liver cancers require efficient single-strand break repair for their growth in order to benefit from a low aldehyde detoxification metabolism. We also propose that the ratio of XRCC1 and ALDH2 levels may serve as a useful prognostic tool in these cancer types.

Keywords: ALDH2; Aldehydes; Base excision repair; DNA damage; Genetic instability; Liver and lung carcinomas; Mithramycin a; XRCC1.

MeSH terms

  • Aldehyde Dehydrogenase, Mitochondrial / genetics
  • Aldehyde Dehydrogenase, Mitochondrial / metabolism*
  • Cell Line
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • DNA Damage / genetics
  • DNA Damage / physiology
  • Humans
  • Liver Neoplasms / genetics
  • Liver Neoplasms / metabolism*
  • Liver Neoplasms / mortality*
  • Lung Neoplasms / genetics
  • Lung Neoplasms / metabolism*
  • Lung Neoplasms / mortality*
  • Plicamycin / analogs & derivatives
  • Plicamycin / pharmacology
  • RNA, Small Interfering / genetics
  • RNA, Small Interfering / physiology
  • X-ray Repair Cross Complementing Protein 1 / antagonists & inhibitors
  • X-ray Repair Cross Complementing Protein 1 / genetics
  • X-ray Repair Cross Complementing Protein 1 / metabolism*

Substances

  • RNA, Small Interfering
  • X-ray Repair Cross Complementing Protein 1
  • XRCC1 protein, human
  • mithramycin A
  • ALDH2 protein, human
  • Aldehyde Dehydrogenase, Mitochondrial
  • Plicamycin