The effects of DLEU1 gene expression in Burkitt lymphoma (BL): potential mechanism of chemoimmunotherapy resistance in BL

Oncotarget. 2017 Apr 25;8(17):27839-27853. doi: 10.18632/oncotarget.15711.

Abstract

Following a multivariant analysis we demonstrated that children and adolescents with Burkitt lymphoma (BL) and a 13q14.3 deletion have a significant decrease in event free survival (EFS) despite identical short intensive multi-agent chemotherapy. However, how this deletion in the 13q14.3 region is associated with a significant decrease in EFS in children and adolescents with BL is largely unknown. The gene Deleted in Lymphocytic Leukemia 1 (DLEU1) is located in the region of 13q14.3. Here, we report that DLEU1 expression is implicated in the regulation of BL programmed cell death, cell proliferation, and expression of apoptotic genes in transcription activator-like effector nuclease (TALEN)s-induced DLEU1 knockdown and DLEU1 overexpressing BL cell lines. Furthermore, NSG mice xenografted with DLEU1 knockdown BL cells had significantly shortened survival (p < 0.05 and p < 0.005), whereas those xenografted with DLEU1 overexpressing BL cells had significantly improved survival (p < 0.05 and p < 0.0001), following treatment with rituximab and/or cyclophosphamide. These data suggest that DLEU1 may in part function as a tumor suppressor gene and confer chemoimmunotherapy resistance in children and adolescents with BL.

Keywords: B-NHL; DLEU1; chemoimmunotherapy; genome editing; tumor suppressor.

MeSH terms

  • Adolescent
  • Animals
  • Antineoplastic Agents / pharmacology*
  • Antineoplastic Agents / therapeutic use
  • Antineoplastic Agents, Immunological / pharmacology
  • Antineoplastic Agents, Immunological / therapeutic use
  • Apoptosis
  • Burkitt Lymphoma / drug therapy*
  • Burkitt Lymphoma / genetics*
  • Burkitt Lymphoma / mortality
  • Burkitt Lymphoma / pathology
  • Cell Line, Tumor
  • Cell Proliferation
  • Child
  • Chromosome Deletion*
  • Chromosomes, Human, Pair 13 / genetics*
  • Cyclophosphamide / pharmacology
  • Cyclophosphamide / therapeutic use
  • Disease-Free Survival
  • Drug Resistance, Neoplasm / genetics*
  • Female
  • Gene Knockdown Techniques
  • Genes, Tumor Suppressor
  • HEK293 Cells
  • Humans
  • Mice
  • Mice, Inbred NOD
  • RNA, Long Noncoding
  • Rituximab / pharmacology
  • Rituximab / therapeutic use
  • Signal Transduction
  • Transcription Activator-Like Effector Nucleases / genetics
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism*
  • Xenograft Model Antitumor Assays

Substances

  • Antineoplastic Agents
  • Antineoplastic Agents, Immunological
  • DLEU1 lncRNA, human
  • RNA, Long Noncoding
  • Tumor Suppressor Proteins
  • Rituximab
  • Cyclophosphamide
  • Transcription Activator-Like Effector Nucleases