CD40L/IL-4-stimulated CLL demonstrates variation in translational regulation of DNA damage response genes including ATM

Blood Adv. 2018 Aug 14;2(15):1869-1881. doi: 10.1182/bloodadvances.2017015560.

Abstract

CD40L/interleukin-4 (IL-4) stimulation occurs in vivo in the tumor microenvironment and induces global translation to varying degrees in individuals with chronic lymphocytic leukemia (CLL) in vitro. However, the implications of CD40L/IL-4 for the translation of specific genes is not known. To determine the most highly translationally regulated genes in response to CD40L/IL-4, we carried out ribosome profiling, a next-generation sequencing method. Significant differences in the translational efficiency of DNA damage response genes, specifically ataxia-telangiectasia-mutated kinase (ATM) and the MRE11/RAD50/NBN (MRN) complex, were observed between patients, suggesting different patterns of translational regulation. We confirmed associations between CD40L/IL-4 response and baseline ATM levels, induction of ATM, and phosphorylation of the ATM targets, p53 and H2AX. X-irradiation was used to demonstrate that CD40L/IL-4 stimulation tended to improve DNA damage repair. Baseline ATM levels, independent of the presence of 11q deletion, correlated with overall survival (OS). Overall, we suggest that there are individual differences in translation of specific genes, including ATM, in response to CD40L/IL-4 and that these interpatient differences might be clinically important.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Ataxia Telangiectasia Mutated Proteins / genetics
  • Ataxia Telangiectasia Mutated Proteins / immunology*
  • CD40 Ligand / genetics
  • CD40 Ligand / immunology*
  • DNA Damage*
  • Female
  • Gamma Rays
  • Histones / genetics
  • Histones / immunology
  • Humans
  • Interleukin-4 / genetics
  • Interleukin-4 / immunology*
  • Leukemia, Lymphocytic, Chronic, B-Cell / immunology*
  • Leukemia, Lymphocytic, Chronic, B-Cell / pathology
  • Male
  • Protein Biosynthesis / genetics
  • Protein Biosynthesis / immunology*
  • Protein Biosynthesis / radiation effects
  • Tumor Microenvironment / genetics
  • Tumor Microenvironment / immunology
  • Tumor Microenvironment / radiation effects
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / immunology

Substances

  • H2AX protein, human
  • Histones
  • IL4 protein, human
  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • CD40 Ligand
  • Interleukin-4
  • ATM protein, human
  • Ataxia Telangiectasia Mutated Proteins