Event Date
⭐️ Presented by the Center for the Advancement of Multicultural Perspectives on Science (CAMPOS)
Jacqueline Barlow
Associate Professor, Microbiology and Molecular Genetics
“G-quadruplex stabilization induces DNA breaks in pericentromeric repetitive DNA sequences in B lymphocytes”
DNA secondary G-quadruplex (G4) structures can impair and even obstruct the DNA replication. Defects in processing G4 structures are associated with replication stress, a common property of both B cell cancers and hyperproliferative premalignant cells. Genome instability arising from replication stress is a hallmark of cancer and strongly contributes to the chromosome rearrangements in B cell cancers. Here, we define the impact of G4 stabilizing ligands on generating genome instability in non-cancerous and malignant B cells. Treatment with the G4-stabilizing compound pyridostatin (PDS) causes breaks and chromosome rearrangements at ribosomal DNA and pericentromeric major satellite regions in both mouse primary B cell cells and CH12 mouse lymphoma cells. Remarkably, PDS causes a high level of tetraploidy correlated with high level of dicentric chromosomes specifically in primary but not in CH12 B cells. Unlike primary B cells, CH12 cells undergo checkpoint activation and strong G2/M arrest in response to PDS treatment thus preventing tetraploid appearance in metaphases. PDS also causes extensive pericentromeric DNA damage in a human Burkitt’s lymphoma cancer cell line. Altogether, these results highlight the difference between primary and malignant B cells in response to PDS, revealing the therapeutic potential of G4-stabilizing drugs to selectively suppress tumor cell growth and proliferation.
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