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SUM159 cells treated with sudemycin D6 (SD6)

ABSTRACT: The objective is to identify gene expression patterns that occur after spliceosome inhibition in triple-negative breast cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE163414 | GEO | 2020/12/18

REPOSITORIES: GEO

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MDA-MB-231-LM2 cells treated with sudemycin D6 (SD6)

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Project description:The objective is to identify splicing changes that occur after spliceosome inhibition in triple-negative breast cancer, specifically in cytoplasmic RNA.

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Expression data from TGFBR3 controls and TGFBR3 knockdown of SUM159 3D cultures

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Expression data from TGFBR3 controls and TGFBR3 knockdown of SUM159 3D cultures

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. Control (N=3) and TGFBR3KD (N=3) samples were hybridized to the Human gene 1.0 ST array, scanned with Affymetrix using AGCC v. 3.2.4 and then analyzed in R 3.0.1 using the oligo package.

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RNA-seq of shE4F1 or shCTRL SUM159 triple negative breast cancer cell line treated or not with Gemcitabine

Project description:E4F1 is a ubiquitously expressed zinc-finger protein of the Gli-Kruppel family that was first identified, more than 30 years ago, as a cellular target of the adenoviral oncoprotein E1A13S (Ad type V), required for transcriptional regulation of adenoviral genes. In this study we investigated the impact of direct translational target genes on DNA damage response induced by Gemcitabine. To do so, we performed RNAseq SUM159 triple negative breast cancer cell line. SUM159 was tranfected either with shE4F1 OR shscramble treated or not with Gemcitabine for 24 hours.

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Transcriptome profiling of SUM159 and derivatives with different metastasis capability

Project description:Triple negative breast cancer cell line SUM159 labeled with triple reporter (TR, TK-GFP-fLUC) injected into Nude mice via mammary fat pad and tail vein injection. Tumor progression is monitored by in vivo bioluminescent imaging. Tumors from mammary and lung were isolated and cultured. These derivatives cells are further tested for their capability to develop mammary primary tumor and metastasis in lung and bone in mice. The total RNA samples are extracted from the panel of SUM159 and derivatives and the transcriptome profiles are determined by microarray. The correlation of transcriptome of the cells to metastasis capability indicated candidate genes and regulatory pathways of metastasis of TNBC.

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High-throughout sequencing of triple negative breast cancer cells treated actived compound D16

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2021-08-17 | GSE182063 | GEO

SUM159 BrCa Decitabine Gene Expression

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

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