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Expression data to identify putative transcriptional targets of ZNF165 in Triple Negative Breast Cancer (TNBC)

ABSTRACT: We found that the cancer testis antigen, ZNF165, is required for viability and can modulate TGFβ-induced gene expression in mesenchymal, Claudin-Low, TNBC. We employed the Affymetrix microarray platform to uncover transcriptionally modulated genes following ZNF165 depletion and TGFβ stimulation using the Claudin-low TNBC tumor-derived cell lines, SUM159 as a model. Our results provide insight into how ZNF165 globally modulates TGFβ signaling. We used microarray analysis to uncover the transcriptional network controlled by ZNF165 and clarify the role of ZNF165 in global TGFβ signaling

ORGANISM(S): Homo sapiens

PROVIDER: GSE63984 | GEO | 2015/11/09

SECONDARY ACCESSION(S): PRJNA269723

REPOSITORIES: GEO

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Expression data to identify putative transcriptional targets of ZNF165 in Triple Negative Breast Cancer (TNBC)

Project description:We found that the cancer testis antigen, ZNF165, is required for viability and can modulate TGFÎ²-induced gene expression in mesenchymal, Claudin-Low, TNBC. We employed the Affymetrix microarray platform to uncover transcriptionally modulated genes following ZNF165 depletion and TGFÎ² stimulation using the Claudin-low TNBC tumor-derived cell lines, SUM159 as a model. Our results provide insight into how ZNF165 globally modulates TGFÎ² signaling. We used microarray analysis to uncover the transcriptional network controlled by ZNF165 and clarify the role of ZNF165 in global TGFÎ² signaling SUM159 and WHIM12 cells were reverse transfected with either non-targeting or ZNF165 siRNA. For SUM159 cells, sixty hours post-transfection, cells were exposed to TGFÎ² for 3 hours. For WHIM12, forty eight hours post-transfection, cells were exposed to TGFÎ² for 3 hours. Total RNA was isolated and hybridized on to Affymetrix microarrays. Each experiment was repeated three times.

2015-11-09 | E-GEOD-63984 | biostudies-arrayexpress

ChIP-Seq analysis to identify direct binding of ZNF165

Project description:We found that the cancer testis antigen, ZNF165, is required for viability and modulates TGFβ-induced gene expression in mesenchymal, Claudin-Low, TNBC. To begin to define ZNF165's role in TNBC tumorigenesis, we performed ChIP-Seq analysis in the mesenchymal TNBC tumor derived cell line, WHIM12, stably expressing ZNF165-V5. This analysis uncovered 381 peaks associated with 410 genes and included TGFβ target genes, SMURF2 and SMAD, that promote negative TGFβ feedback regulation. Our results provide insight into how ZNF165 globally modulates TGFβ signaling and nominates ZNF165 candidate gene targets.

2015-11-09 | GSE65937 | GEO

Genomic binding profiles for ZNF165, ZNF446, and SMAD3 in triple-negative breast cancer

Project description:The testis protein ZNF165 is aberrantly expressed in triple-negative breast cancer (TNBC), where it modulates TGFβ signaling to promote tumor growth and survival. To investigate whether ZNF165 functions in this capacity via cooperation with SMAD3, a canonical TGFβ-induced transcription factor, we performed ChIP-seq for both factors in TNBC cell lines (WHIM12 and SUM159). Additionally, we established genomic binding profiles for ZNF446, a previously uncharacterized transcription factor that we have identified as a member of a ZNF165-SMAD3 complex.

2020-06-10 | GSE130364 | GEO

ChIP-Seq analysis to identify direct binding of ZNF165

Project description:We found that the cancer testis antigen, ZNF165, is required for viability and modulates TGFÎ²-induced gene expression in mesenchymal, Claudin-Low, TNBC. To begin to define ZNF165's role in TNBC tumorigenesis, we performed ChIP-Seq analysis in the mesenchymal TNBC tumor derived cell line, WHIM12, stably expressing ZNF165-V5. This analysis uncovered 381 peaks associated with 410 genes and included TGFÎ² target genes, SMURF2 and SMAD, that promote negative TGFÎ² feedback regulation. Our results provide insight into how ZNF165 globally modulates TGFÎ² signaling and nominates ZNF165 candidate gene targets. WHIM12 cells were stably infected ZNF165-V5 were grown to 75% confluency. Chromatin was isolated, sonicated and immunoprecipitated using a V5 antibody. Purifed ChIP-ed DNA was then sequence, aligned to hg19 and HOMER was justed to identify significantly enriched peaks.

2015-11-09 | E-GEOD-65937 | biostudies-arrayexpress

Transcriptomes of triple-negative breast cancer (TNBC) cells (SUM159) and non-TNBC cells (HCC1569) that overexpressed JMJD6 were compared

Project description:The expression levels of JMJD6 and its correlation with H2A.XY39ph differed in TNBC and non-TNBC cells. In addition, we have previously shown that H2A.XY39ph levels are positively correlated with tumor size, histological grade and advanced TNM stage in breast cancer. To analyze the role of JMJD6 in regulating the characteristics of different subtypes of breast cancer, the transcriptomes of TNBC cells (SUM159) and non-TNBC cells (HCC1569) that overexpressed JMJD6 were compared. We speculate that JMJD6 overexpression cause autophagy pathway activation in TNBC via enhancing ATG genes expression.

2023-10-01 | E-MTAB-6517 | biostudies-arrayexpress

Human TNBC Cells 72h Treatment with 4.5nM OTSSP167 MELK Inhibitor vs. DMSO Control (SUM159)

Project description:Microarray comparing TNBC cells treated for 72 hours with OTSSP167 MELK Inhibitor and control (DMSO) Two-condition arrays: SUM159 cells were treated with either 4.5nM OTSSP167 MELK Inhibitor or 0.045% DMSO for 72h. Two biological replicates, one per array, with a dye swap (technical replicate).

2017-05-01 | E-GEOD-71026 | biostudies-arrayexpress

Human TNBC Cells 72h Treatment with 45nM OTSSP167 MELK Inhibitor vs. DMSO Control (SUM159)

Project description:Microarray comparing TNBC cells treated for 72 hours with OTSSP167 MELK Inhibitor and control (DMSO) Two-condition arrays: SUM159 cells were treated with either 45nM OTSSP167 MELK Inhibitor or 0.045% DMSO for 72h. Two biological replicates, one per array, with a dye swap (technical replicate).

2017-05-01 | E-GEOD-71027 | biostudies-arrayexpress

Tubacin mediates the synthetic lethality of cysteine in breast cancer independent on HDAC6

Project description:Triple-negative breast cancer (TNBC) has a highly aggressive nature and distinct molecular characteristics from other subtypes of breast cancer and lacks effective targeted therapy. The molecular and genetic basis of cysteine/cystine dependency in TNBC is complex. We found that cysteine addiction associates with the expression of a set of Claudin genes in TNBC. The Claudin-high TNBCs are independent on cystine, while the Claudin-low TNBCs undergo rapid ferroptosis upon cystine deprivation or inhibition of cystine transport by erastin. To overcome the resistance of Claudin-high TNBC and luminal breast cancer to the potential targeted cystine-addiction therapy, we explored the synthetic lethality of cysteine by an epigenetic compound library screen. Several potent HDAC6 inhibitors were identified and rendered the Claudin-high TNBCs and luminal cancer cells dependent on extracellular cystine and undergoing ferroptosis upon cystine deprivation. The transcriptomic profiling showed that the HDAC6 inhibitor tubacin in combination with erastin activates a synthetic-lethal transcriptional program. Together, we have identified the HDAC6 inhibitors as potent therapy-sensitizers to revive the targeted cysteine-addiction therapy for various subtypes of breast cancer, not limit in the Claudin-low TNBC.

2021-06-02 | GSE154425 | GEO

LncRNA expression profile in triple negative breast cancer (TNBC)

Project description:To identify novel TNBC-relevant lncRNAs, we performed lncRNA microarray analysis using 5 TNBC tissues and their matched adjacent non-cancerous tissues by Arraystar Human LncRNA Microarray V3.0.

2021-07-01 | GSE156144 | GEO

TGFβ/Cyclin D1/Smad-mediated inhibition of BMP4 promotes breast cancer stem cell self-renewal activity

Project description:To understand the mechanism by which TGFβ regulates tumor initiation in triple negative breast cancer (TNBC), we performed microarray analysis using Illumina Human HT-12 Gene Expression BeadChip. A TNBC cell line of SCP2 was treated or not with TGFβ for 24 hours. Differentially expressed genes were analyzed by comparing treated versus non-treated samples

2021-12-27 | GSE163883 | GEO

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