Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profile at single cell level of BT-549 TNBC Spheroid cultures with inducible expression of CTL or MUC1 targeting knockdown

ABSTRACT: The MUC1-C protein evolved in mammals for adaptation of barrier tissues to loss of homeostasis. Prolonged activation of MUC1-C in settings of chronic inflammation promotes lineage plasticity, epigenetic reprogramming and the cancer stem cell (CSC) state. The effects of MUC1-C on the metabolism of CSCs remain unexplored. We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of BT-549 spheroid cultures with and without knockdown of MUC1 to examine the effects of MUC1 on CSC renewal and metbolic states.

ORGANISM(S): Homo sapiens

PROVIDER: GSE230308 | GEO | 2023/11/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Identification of methylated sites in BT-549 cells affected by thymoquinone treatment

Project description:BT-549 cells were treated with thymoquinone for 6 h and chromatin immune-precipitation (ChIP) was performed using anti- MBD1 antibody (Abcam, USA). Anti-MBD1 could precipitate specific genomic region, which are methylated. The ChIP products were sequenced by library construction and bioinformatics analysis. The gene ontology (GO) analysis for multiple pathways was performed. The genomic methylated regions affected by TQ treatment were identified.

2022-06-15 | GSE178334 | GEO

Restoring miR-150-5p to a triple negative breast cancer cell line [BT-549]

Project description:The objective of these experiments is to identify novel direct and indirect targets of miR-150-5p in breast cancer cell lines. The goal is that these will give direction as to what targets or pathways may be contributing to the reduced growth observed in these cell lines upon restoration of miR-150-5p. A therapy directed towards one or more critical subtype-specific targets could be developed as a therapeutic for breast cancer patients. Using has-miR-150-5p mirVana miRNA mimic (Ambion, 4464066), miR-150-5p was restored to a triple negative breast cancer cell line, BT-549.

2017-01-01 | GSE87589 | GEO

microRNA profiling of luminal and TNBC breast cancer cell lines

Project description:two luminal cell lines were added, MCF7 and BT-474 two TNBC cell line were added, MB231 and BT-549

2014-10-03 | GSE62022 | GEO

RNA-Sequencing analysis of Meox1 siRNA knockdown in p53 and PTEN deficient triple negative breast cancer in vitro cell lines of BT-549 and MDA-MB-468

Project description:The goal for this experiment was to analyze how knockdown of homeobox transcription factor Meox1 altered functional and mechanist biology of p53 and PTEN deficient triple negative breast cancer in vitro cell lines of claudin-low BT-549 and basal-like MDA-MB-468.

2020-05-26 | GSE133927 | GEO

microRNA profiling of luminal and TNBC breast cancer cell lines

Project description:two luminal cell lines were added, MCF7 and BT-474 two TNBC cell line were added, MB231 and BT-549 microRNA expression profiles were conpared between the luminal group and the TNBC group

2014-10-03 | E-GEOD-62022 | biostudies-arrayexpress

Transcriptome analysis for CT mRNA treated BT-549 cells and negative control cells

Project description:We report the altered metabolite changes by processing CT mRNA in the TNBC cell line, BT-549. It was confirmed that the treatment of CT mRNA disrupted the synthesis of dTTP during nucleic acid metabolism, increasing the signal related to DNA damage in the cell, and that the energy metabolism and NADPH metabolism in the cell were changed for its recovery. The main energy sources, glucose metabolism and glutamine metabolism, are closely linked to the mitochondrial TCA cycle products. In the CT mRNA treatment group, intracellular nucleic acid depletion was observed to increase glutamine metabolism as a source of N source, and the pathway of aspartate utilization was observed. It was confirmed that it was expanded. As a result, a significant increase in the cysteine influx was observed according to the occurrence of ROS, and an effort to regulate the intracellular NADPH balance was observed through the change of metabolites over time. Finally, it was observed that the oncogenic pathway was significantly reduced in the CT mRNA-treated group compared with all untreated groups or controls with other substrate specificities. This study characterizes changes in intracellular metabolites caused by specific dTTP biosynthesis disturbances.

2022-05-07 | GSE202194 | GEO

MUC1-C integrates induction of aerobic glycolysis with suppression of oxidative phosphorylation in cancer stem cells

Project description:The MUC1-C protein evolved in mammals for adaptation of barrier tissues to loss of homeostasis. Prolonged activation of MUC1-C in settings of chronic inflammation promotes lineage plasticity, epigenetic reprogramming and the cancer stem cell (CSC) state. The effects of MUC1-C on the metabolism of CSCs remain unexplored. The present studies performed on purified populations of triple-negative breast cancer (TNBC) CSCs demonstrate that MUC1-C integrates the capacity for self-renewal with the activation of aerobic glycolysis. We show that MUC1-C is essential for (i) CSC mammosphere formation and tumorigenicity and (ii) activation of GLUT1, HK2 and other glycolytic genes. We further show that MUC1-C activates nuclear genes that encode components of mitochondrial Complexes II-V of the electron transfer chain (ETC). Of importance, MUC1-C also represses mitochondrial DNA (mtDNA) genes encoding components of Complexes I-V. The observed involvement of MUC1-C in the suppression of mtDNA genes is explained by MUC1-C-mediated (i) downregulation of the mitochondrial transcription factor A (TFAM), which is required for mtDNA transcription, and (ii) induction of the mitochondrial transcription termination factor 3 (mTERF3). In support of this pathway to suppress mitochondrial ROS production, targeting MUC1-C increases (i) mtDNA gene transcription, (ii) superoxide levels and (iii) loss of self-renewal capacity. These findings indicate that MUC1-C regulates CSC self-renewal and redox balance by integrating activation of glycolysis with suppression of oxidative phosphorylation.

2023-10-11 | GSE222377 | GEO

Identification of methylated sites in BT-549 cells affected by thymoquinone treatment

Project description:Identification of methylated sites in BT-549 cells affected by thymoquinone treatment

| PRJNA738509 | ENA

MUC1-C INDUCES PBRM1-MEDIATED CHROMATIN REMODELING IN DRIVING CHRONIC INFLAMMATION AND DNA DAMAGE RESISTANCE IN TRIPLE-NEGATIVE BREAST CANCER [tet-MUC1 shRNA]

Project description:STAT1 and IRF1 are essential effectors of the type I and II interferon (IFN) pathways. Here, we report that the oncogenic MUC1-C protein is necessary for inducing chromatin accessibility and activation of the STAT1 and IRF1 genes in triple-negative breast cancer (TNBC) cells. Our results demonstrate that MUC1-C activates the PBRM1 subunit of the SWI/SNF PBAF chromatin remodeling complex and forms a nuclear complex with PBRM1. We show that MUC1-C associates with PBRM1 and STAT1 on the IRF1 gene at (i) a proximal enhancer-like signature (PLS), and (ii) distal enhancer-like signatures (dELSs). We also show MUC1-C and PBRM1 are necessary for opening chromatin at these signatures and for the induction of IRF1 expression. In extending these results, we found that MUC1-C binds directly to IRF1 and forms nuclear complexes with PBRM1 and IRF1, which are necessary for inducing chromatin accessibility at PLS of the (i) STAT1 gene, (ii) type II IFN pathway IDO1 and WARS genes, and (iii) type I IFN pathway RIG-I, MDA5 and ISG15 genes. Consistent with involvement of chronic inflammation in promoting the cancer stem cell (CSC) state, we show that MUC1-C, PBRM1 and IRF1 are required for self-renewal of TNBC CSCs. Of translational relevance, we report that targeting MUC1-C, PBRM1 and IRF1 circumvents intrinsic DNA damage resistance of TNBC CSCs and that MUC1-C is necessary for acquired resistance to the PARP inhibitor olaparib. These findings demonstrate that MUC1-C activates PBRM1/IRF1 and thereby chromatin remodeling of IFN pathway genes that promote chronic inflammation, the CSC state and DNA damage resistance.

2023-06-14 | GSE212587 | GEO

Transcriptome analysis for CT mRNA treated BT-549 cells and negative control cells

Project description:Transcriptome analysis for CT mRNA treated BT-549 cells and negative control cells

| PRJNA834969 | ENA