SUM159 BrCa Decitabine Gene Expression
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ABSTRACT:
PROVIDER: PRJNA553252 | ENA |
REPOSITORIES: ENA
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Project description:Dysregulation of DNA methylation is an established feature of breast cancers. DNA demethylating therapies like decitabine are proposed for the treatment of triple-negative breast cancers (TNBCs) and indicators of response need to be identified. For this purpose, we characterized the effects of decitabine in a panel of 10 breast cancer cell lines and observed a range of sensitivity to decitabine that was not subtype-specific. Knockdown of potential key effectors demonstrated the requirement of deoxycytidine kinase (DCK) for decitabine response in breast cancer cells. In treatment-naive breast tumors, DCK was higher in TNBCs, and DCK levels were sustained or increased post chemotherapy treatment. This suggests that limited DCK levels will not be a barrier to response in TNBC patients treated with decitabine as a second line treatment or in a clinical trial. Methylome analysis revealed that genome-wide, region-specific, tumor suppressor gene-specific methylation, and decitabine-induced demethylation did not predict response to decitabine. Gene set enrichment analysis (GSEA) of transcriptome data demonstrated that decitabine induced genes within apoptosis, cell cycle, stress, and immune pathways in decitabine treated cells. Induced genes included those characterized by the viral mimicry response; however knockdown of key effectors of the pathway did not affect decitabine sensitivity suggesting that breast cancer growth suppression by decitabine is independent of viral mimicry. Finally, taxol-resistant breast cancer cells expressing high levels of multidrug resistance transporter ABCB1 remained sensitive to decitabine, suggesting that the drug could be used as second-line treatment for chemoresistant patients. We used microarrays to determine genome-wide expression changes induced by DNA de-methylating agent decitabine in breast cancer cell lines
2020-06-01 | GSE133987 | GEO
Project description:To investigate the role of iNOS in tumor cell morphology and gene expression, we utilized CRISPR-Cas9 gene editing (NOS2 Double Nickase Plasmid, Santa Cruz) to knockout NOS2 in SUM159 cells. After puromycin selection, resistant clones were selected by immunoblotting for iNOS expression and nitrite/nitrate colorimetric assay. We then performed gene expression profiling analysis using data obtained from RNA-seq of parental SUM159 cells compared to NOS2KO SUM159 cells.
2024-05-28 | GSE234512 | GEO
Project description:To globally evaluate transcriptome in THP-1 and decitabine-resistant THP-1 cells treated by decitabine, cells were treated with the IC90 dose of decitabine until 90% cell death was reached, then cultured in decitabine-free medium until confluence, followed by another round of decitabine treatment and the treatment cycles were repeated for 3 months to generate decitabine-resistant THP-1 cells. We then performed gene expression profiling analysis using data obtained from RNA-seq of THP-1 or decitabine-resistant THP-1 cells treated with or without decitabine.
2025-06-28 | GSE269185 | GEO
Project description:The objective of this experiment was to determine global gene expression change in triple negative cell line upon knockdown of TGFBR3. Genotype specific differences in expression profiles have been evaluated using human HuGene1.0-ST affymetrix array. RNA was extracted from SUM159 controls and SUM159 TGFBR3KD cells cultured in 3-dimensional in vitro system.
2014-02-06 | GSE54756 | GEO
Project description:We used a transmitochondrial cybrid (cybrids)-based discovery approach to identify mitochondria-regulated cancer pathways in TN BCa. Cybrids were generated under a moderately metastatic TN BCa cell line SUM159 as the common nuclear background with mitochondria from benign breast epithelium (A1N4) and moderately metastatic (SUM159) TN BCa cells. In vitro and in vivo studies suggested that even under the common moderately cancerous nuclear background, mitochondria from benign cells inhibit and metastatic cell induce cancer properties of a moderately aggressive TN BCa cell. Gene expression studies identified c-Src onco-pathway as one of the major cancer pathways altered according to the mitochondria status of the cybrids. SUM159 Ï0 cells were used as nuclear donor and A1N4 and SUM 159 cells were used as mitochondrial donor cells. The two groups were profiled for gene expression using microarrays. two group comparison (159/SUM159 vs A1/SUM159)
2016-04-14 | E-GEOD-72319 | biostudies-arrayexpress
Project description:Acute myeloid leukemia (AML), and other myeloid malignancies, are frequently treated with hypomethylating agents like decitabine. Alterations in the epigenome, induced by decitabine, are likely to result in gene expression changes. The effects of decitabine have not been systemically studied using primary AML samples. We cultured 18 different primary AML samples for 7 days, the last 3 days of which included 100 nM decitabine (DAC) or 100 nm cytarabine (AraC). We hypothesized that decitabine treatment would result in detectable and consistent gene expression changes. For comparison, we also analyzed mRNA from cells treated with DMSO control (mock) and mRNA from uncultured cells taken at the time of diagnosis.
2012-12-18 | E-GEOD-40442 | biostudies-arrayexpress
Project description:We used a transmitochondrial cybrid (cybrids)-based discovery approach to identify mitochondria-regulated cancer pathways in TN BCa. Cybrids were generated under a moderately metastatic TN BCa cell line SUM159 as the common nuclear background with mitochondria from benign breast epithelium (A1N4) and moderately metastatic (SUM159) TN BCa cells. In vitro and in vivo studies suggested that even under the common moderately cancerous nuclear background, mitochondria from benign cells inhibit and metastatic cell induce cancer properties of a moderately aggressive TN BCa cell. Gene expression studies identified c-Src onco-pathway as one of the major cancer pathways altered according to the mitochondria status of the cybrids.
2016-04-14 | GSE72319 | GEO
Project description:Acute myeloid leukemia (AML), and other myeloid malignancies, are frequently treated with hypomethylating agents like decitabine. Alterations in the epigenome, induced by decitabine, are likely to result in gene expression changes. The effects of decitabine have not been systemically studied using primary AML samples.
2012-12-18 | GSE40442 | GEO
Project description:Rare melanoma subtypes, including mucosal melanoma, can exhibit reduced tumor-intrinsic innate immune and interferon-associated gene expression, which may contribute to immune evasion and limited responses to immune checkpoint inhibitors. We investigated whether decitabine, a DNA methyltransferase inhibitor known to induce viral mimicry and immune-associated transcriptional programs, could restore innate immune and interferon-associated signaling in rare melanomas. Here, we report RNA-seq profiling of the MB2141 anorectal mucosal melanoma model following decitabine treatment in vitro and in vivo. Decitabine treatment resulted in robust induction of innate immune pathogen sensing, type I interferon signaling, antigen presentation, and other immune-associated gene expression programs. These data provide a transcriptional framework for understanding how DNA hypomethylating agents modulate immune gene expression in mucosal melanoma and support further investigation of decitabine as an immune-priming strategy for rare melanoma subtypes.
2026-07-13 | GSE337536 | GEO
Project description:We conducted RNA sequencing of SUM159 DAPK3 KO and control cells followed by Gene Set Enrichment Analysis (GSEA) to identify altered gene expression pathways by DAPK3 knockout. Epithelial-mesenchymal transition (EMT) pathway was the top significantly down-regulated pathway in SUM159 DAPK3 KO cells as compared to control cells.
2024-10-10 | GSE273142 | GEO