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Expression data for T47D cells treated with 2mM hydroxyurea

ABSTRACT: RAD51B, a paralog of RAD51, have been associated with breast cancer risk in genome-wide association studies. The underlying biological mechanism through which germline genetic variation in RAD51B confers susceptibility to breast cancer is not well understood. Here we investigate the molecular function of RAD51B in breast cancer cell lines. We used microarrays to detail the global gene expression to identify classes of genes that are regulated differnetly post DNA damages as a result of RAD51B depeletion.

ORGANISM(S): Homo sapiens

PROVIDER: GSE56940 | GEO | 2014/04/22

SECONDARY ACCESSION(S): PRJNA245032

REPOSITORIES: GEO

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Expression data for T47D cells treated with 2mM hydroxyurea

Project description:RAD51B, a paralog of RAD51, have been associated with breast cancer risk in genome-wide association studies. The underlying biological mechanism through which germline genetic variation in RAD51B confers susceptibility to breast cancer is not well understood. Here we investigate the molecular function of RAD51B in breast cancer cell lines. We used microarrays to detail the global gene expression to identify classes of genes that are regulated differnetly post DNA damages as a result of RAD51B depeletion. T47D cells were first transfected with either non-targeting (control; siCON) or RAD51B-targeting (experimental; siRAD51B) siRNA, then followed by 24hr treatment of 2mM hydroxyurea (HU). Total RNA were extracted at the end of the treatment for microarray analysis. Three biological replicates were carried out for both control and experimental samples.

2014-04-22 | E-GEOD-56940 | biostudies-arrayexpress

Expression data for T47D cells treated with 2mM hydroxyurea

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Project description:Whole chromosome losses resulting in near-haploid karyotypes are found in a rare subgroup of treatment-refractory acute lymphoblastic leukemia. To systematically dissect the unique physiology and uncover susceptibilities that can be exploited in near-haploid leukemia, we leveraged single-cell transcriptomics and computational inference of cell cycle stages to pinpoint key differences between near-haploid and diploid leukemia cells. Combining cell cycle stage-specific differential expression with gene essentiality metrics obtained from a genome-wide CRISPR-Cas9-mediated knockout screen, we identified the homologous recombination pathway component RAD51B as an essential gene in near-haploid leukemia. DNA damage analyses revealed significantly increased sensitivity of RAD51-mediated repair to RAD51B loss in the G2/M stage of near-haploid cells, suggesting a unique role of RAD51B in the homologous recombination pathway. We observed elevated G2/M checkpoint signaling as well as a RAD51B signature expression program in response to chemotherapy in a xenograft model of human near-haploid B-ALL, as well as overexpression of RAD51B and its associated programs in a large panel of near-haploid B-ALL patients. These data highlight a unique genetic dependency on DNA repair machinery in near-haploid leukemia and demarcate RAD51B as a promising candidate for targeted therapy in this treatment-resistant disease.

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