Biglycan and reduced glycolysis are associated with breast cancer cell dormancy in the brain
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA908080 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22515589_1.fastq.gz | Fastqsanger.gz | |||
| SRR22515589_2.fastq.gz | Fastqsanger.gz | |||
| SRR22515590_1.fastq.gz | Fastqsanger.gz | |||
| SRR22515590_2.fastq.gz | Fastqsanger.gz | |||
| SRR22515591_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:To understand the mechanisms of breast cancer cell dormancy in the brain
2023-06-29 | GSE220017 | GEO
Project description:To determine genes involved in induction of dormancy in response to reduced maturation temperatures, RNA sequencing was performed on developing seeds matured at 20°C, where low dormancy is observed, and compared to seeds matured at 15°C where high dormancy is observed.
2014-09-04 | GSE61061 | GEO
Project description:We show that the epithelial-like and mesenchymal-like subpopulations of breast cancer stem-like cells (BCSCs) demonstrate different levels dormancy and tumorigenicity in lungs. The long non-coding RNA (lncRNA) molecule NR2F1-AS1 (NAS1) is up-regulated in the dormant BCSC subpopulation, and functionally promotes tumor dissemination but reduces proliferation in lungs. Mechanically, NAS1 promotes internal ribosome entry site (IRES)-mediated NR2F1 translation, leading to inhibition of ΔNp63 transcription by NR2F1. Further, ΔNp63 downregulation results in epithelial-mesenchymal transition, reduced tumorigenicity and enhanced dormancy of cancer cells in lungs.
2023-04-23 | GSE149265 | GEO
Project description:To determine genes involved in induction of dormancy in response to reduced maturation temperatures, RNA sequencing was performed on developing seeds matured at 20°C, where low dormancy is observed, and compared to seeds matured at 15°C where high dormancy is observed. Col green cotyledon seeds matured at 20°C and 15°C were dissected from siliques between five to seven hours after dawn and frozen in liquid nitrogen. RNA was extracted as described previously (Penfield et al., 2005).
2014-09-04 | E-GEOD-61061 | biostudies-arrayexpress
Project description:Breast cancer patients with estrogen receptor positive tumors face a constant risk of disease recurrence for the remainder of their lives. Dormant tumor cells residing in tissues such as the bone marrow may generate clinically significant metastases many years after initial diagnosis. Previous studies suggest that dormant cells display “stem like” properties (CSCs), which may be regulated by the immune system. Although many studies have examined tumor cell intrinsic characteristics of dormancy, the role of the immune system in controlling dormancy and its escape is not well understood. This scientific gap is due, in part, to a lack of immunocompetent mouse models of breast cancer dormancy with many studies involving human xenografts in immunodeficient mice. To overcome this limitation, we studied dormancy in immunocompetent, syngeneic mouse breast cancer models. We find that PyMT, Met-1 and D2.0R cell lines contain CSCs that display both short- and long-term metastatic dormancy in vivo, which is dependent on the host immune system. Natural killer cells were key for the metastatic dormancy phenotype observed for D2.0R and the role of NK cells in regulating CSCs was further investigated. Quiescent D2.0R CSC are resistant to NK cytotoxicity, while proliferative D2.0R CSC were sensitive to NK cytotoxicity both in vitro and in vivo. This resistance was mediated, in part, by the expression of Bach1 and Sox2 transcription factors. NK killing was enhanced by the STING agonist MSA-2. Collectively, our findings demonstrate the important role of immune regulation of breast tumor dormancy and highlight the importance of utilizing immunocompetent models to study this phenomenon.
2024-05-15 | GSE267583 | GEO
Project description:In the present study, we developed a chemical method to produce dihydro nicotinamide mononucleotide (NMNH), which is the reduced-form of nicotinamide mononucleotide (NMN). We demonstrated that NMNH was a better nicotinamide adenine dinucleotide (NAD+) enhancer compared to NMN both in vitro and in vivo mediated by mononucleotide adenylyltransferase (NMNAT). Additionally, NMNH increased the reduced NAD (NADH) levels in cells and in mouse liver. Metabolomic analysis revealed that NMNH inhibited glycolysis and TCA cycle. In vitro experiments demonstrated that NMNH induced cell cycle arrest and suppressed cell growth. Nevertheless, NMNH treatment did not cause observable difference in mice. Taken together, our work demonstrates that NMNH is a potent NAD+ enhancer, and suppresses glycometabolism and cell growth.
2022-02-25 | PXD022547 | Pride
Project description:By entering a reversible state of reduced metabolic activity, dormant microorganisms are able to contend with suboptimal conditions that would otherwise reduce their fitness. In addition, certain types of dormancy like sporulation, can serve as a refuge from parasitic infections. Phages are unable to attach to spores, but their genomes can be entrapped in the resting structures and are able to resume infection upon host germination. Thus, dormancy has the potential to affect both the reproductive and survival components of phage fitness. Here, we characterized the distribution and diversity of sigma factors in nearly 3,500 phage genomes. Homologs of bacterial sigma factors that are responsible for directing transcription during sporulation were preferentially recovered in phages that infect spore-forming hosts. While non-essential for lytic infection, when expressed in Bacillus subtilis, we demonstrate that phage-encoded sigma factors activated sporulation gene networks and reduced spore yield. Our findings suggest that the acquisition of host-like transcriptional regulators may allow phages to manipulate the expression of complex traits, like the transitions involved in bacterial dormancy.
2021-11-05 | GSE187004 | GEO
Project description:These data represent the expression patterns of Mycobacterium tuberculosis in progressive hypoxia, nutrient depletion, and in-vivo hollow fiber models of dormancy. The assumptions are that the set of genes that respond to INH treatment during Log phase growth would not be differentially regulated during INH treatment in the dormancy models, and that the overall number of differentially regulated genes would be reduced do to the low metabolic state of the cells. Keywords: Dormancy Model Drug Response Comparison
2007-12-14 | GSE9776 | GEO
Project description:For many breast cancer (BCa) patients, symptomatic bone metastases appear after years or even decades of latency. How metastatic cells disseminate, and how micrometastatic lesions remain dormant and undetectable yet initiate colonization, are major questions in cancer research. Here we identify and functionally analyse a molecular mechanism involved in bone metastatic latency of estrogen receptor–positive (ER)+ BCa. We developed an in vivo loss-of-function, genome-wide shRNA screening to identify genes relevant for long-latent relapse in BCa. This screen revealed the kinase MSK1 as an important regulator of metastatic dormancy. Importantly, low MSK1 expression associates with early metastasis in ER+ BCa patients. Reduced MSK1 levels impaired cellular differentiation and increased the bone homing and growth capacity of metastatic cells. MSK1 modulates chromatin status at promoters to regulate the expression of luminal differentiation genes, including those for the GATA-3 and FOXA1 transcription factors, which prevent the progression of ER+ BCa towards metastasis. Our results identify the regulation of luminal cell differentiation by MSK1 via modulation of chromatin remodelling to be a key mechanism for controlling metastatic dormancy in BCa. We propose that MSK1 could be a useful marker for stratifying BCa patients as high- or low-risk for early relapse, allowing patients to receive appropriate treatments.
2017-11-13 | GSE100306 | GEO
Project description:Short term transition to high-fat diet (HFD) feeding causes rapid changes in the molecular architecture of the blood-brain-barrier (BBB), BBB permeability and brain glucose uptake. However, the precise mechanisms responsible for these changes remain elusive. Here we detected a rapid downregulation of Notch signaling after short-term HFD feeding. Conversely, Notch activation restores HFD-fed mouse serum induced reduction of Glut1 expression and glycolysis in cultured brain microvascular endothelial cells (BMECs). Selective, inducible expression of Notch-intracellular domain (IC) in BMECs prevents HFD-induced reduction of Glut1 expression and hypothalamic glucose uptake. Caveolin (Cav)-1 expression in BMECs is increased upon short term HFD feeding. However, NotchICBMECs mice display reduced caveola formation and BBB permeability. This ultimately translates into reduced hypothalamic insulin transport, action and systemic insulin sensitivity. Collectively, we highlight a critical role of Notch-signaling in the pleiotropic effects of short-term dietary transitions on BBB functionality.
2025-04-01 | GSE210620 | GEO