Similar Datasets
Project description:Genome wide transcript and target gene profiling reveal that FOXP1 acts directly and indirectly by enforcing known ABC-DLBCL hallmarks, including Chronically Activated B cell receptor Signaling (CABS) and the classical NF-κB survival pathway. Our data further suggest that FOXP1 maintains ABC-subtype distinction by repressing gene expression programs dominant in GCB-DLBCL and support a model in which the normally transitory B cell plasmablast is the target of ABC-DLBCL transformation. ChIP sequenicng was performed for the FOXP1 transcription factor in DLBCL cell lines. Input was sequenced and used as a control.
2016-07-05 | E-GEOD-63257 | biostudies-arrayexpress
Project description:Despite advances in cancer therapy, drug resistance remains a major obstacle in a range of cancer types, often driven by overexpression of ATP-binding cassette (ABC) transporters that restrict intracellular drug accumulation. Our previous studies identified the BRG1-p300 transcriptional complex at the promoters of specific ABC transporter genes. We used basal and induced doxorubicin-resistant triple-negative breast cancer (TNBC) cell lines to analyze changes in ABC transporter expression and drug accumulation following PARP1 inhibition. Moreover, the effect of commonly used antioxidants on the repressive effect of Veliparib against ABC genes was verified. ChIP-Seq was performed to identify transcription factor mediating PARP1-dependent ABC gene regulation. PARP1 inhibition or silencing of PARP1/HPF1 complex components downregulated ABCC and ABCG2 transporters, leading to increased intracellular accumulation of chemotherapeutic drugs in doxorubicin-resistant cells. Notably, suppression of genotoxic stress via antioxidant treatment reverses the inhibitory effect of Veliparib on ABC transporter expression. We identified SMARCA1 as a key regulator of PARP1-dependent expression of ABCC genes. SMARCA1 is a key effector of PARP1/p300-mediated regulation of ABC transporters and represents a potential therapeutic target in doxorubicin-resistant TNBC. These findings support the development of combinatorial strategies involving PARP1 inhibitors and chromatin remodeling modulators in refractory breast cancers.
2025-12-04 | GSE312254 | GEO
Project description:Despite advances in cancer therapy, drug resistance remains a major obstacle in a range of cancer types, often driven by overexpression of ATP-binding cassette (ABC) transporters that restrict intracellular drug accumulation. Our previous studies identified the BRG1-p300 transcriptional complex at the promoters of specific ABC transporter genes. We used basal and induced doxorubicin-resistant triple-negative breast cancer (TNBC) cell lines to analyze changes in ABC transporter expression and drug accumulation following PARP1 inhibition. Moreover, the effect of commonly used antioxidants on the repressive effect of Veliparib against ABC genes was verified. ChIP-Seq was performed to identify transcription factor mediating PARP1-dependent ABC gene regulation. PARP1 inhibition or silencing of PARP1/HPF1 complex components downregulated ABCC and ABCG2 transporters, leading to increased intracellular accumulation of chemotherapeutic drugs in doxorubicin-resistant cells. Notably, suppression of genotoxic stress via antioxidant treatment reverses the inhibitory effect of Veliparib on ABC transporter expression. We identified SMARCA1 as a key regulator of PARP1-dependent expression of ABCC genes. SMARCA1 is a key effector of PARP1/p300-mediated regulation of ABC transporters and represents a potential therapeutic target in doxorubicin-resistant TNBC. These findings support the development of combinatorial strategies involving PARP1 inhibitors and chromatin remodeling modulators in refractory breast cancers.
2025-12-04 | GSE312249 | GEO
Project description:Diffuse large B-cell lymphoma (DLBCL) is the most common non-Hodgkin lymphoma, including two main molecular subtypes termed activated B cell-like (ABC) and germinal center B cell-like (GCB). ABC DLBCL is less curable and identification of new molecular targets is needed for the development of effective therapeutic agents. Here, we focused on EGR1, a transcription factor that is regulated by the B cell receptor and JAK1/STAT3 signaling pathway in ABC DLBCL. ChIP-Seq and RNA-Seq analyses revealed that gene regulation by EGR1 in ABC DLBCL accentuates multiple oncogenic pathways, including MYC and E2F, while dampening the lethal type I IFN pathway.
2021-08-06 | GSE123291 | GEO
Project description:Genome wide transcript and target gene profiling reveal that FOXP1 acts directly and indirectly by enforcing known ABC-DLBCL hallmarks, including Chronically Activated B cell receptor Signaling (CABS) and the classical NF-κB survival pathway. Our data further suggest that FOXP1 maintains ABC-subtype distinction by repressing gene expression programs dominant in GCB-DLBCL and support a model in which the normally transitory B cell plasmablast is the target of ABC-DLBCL transformation.
2016-01-03 | GSE63257 | GEO