Activation of recombinational repair in Ewing sarcoma cells carrying EWS-FLI1 fusion gene by chromosome translocation.

ABSTRACT: Chromosome translocation (TL) is an important mode of genomic changes underlying human tumorigenesis, the detailed mechanisms of which are, however, still not well understood. The two major modalities of DNA double strand break repair, i.e. homologous recombination (HR) and non-homologous end-joining (NHEJ), have been hypothesized. In a typical TL⁺ human neoplasm, Ewing sarcoma, which is frequently associated with t(11;22) TL encoding the EWS-FLI1 fusion gene, NHEJ has been regarded as a model to explain the disease-specific TL. Using comprehensive microarray approaches, we observed that expression of the HR genes, particularly of RAD51, is upregulated in TL⁺ Ewing sarcoma cell lines, WE-68 and SK-N-MC, as in the other TL⁺ tumor cell lines and one defective

SUBMITTER: Tanaka K 

PROVIDER: S-EPMC9427769 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature