Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA125241 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional profiling of MC3T3-E1 osteoblasts that were flow cytometry-separated from cocultures with control or Jagged1-overexpressing tumor cells and treated with either DMSO control or 1μM MRK-003 (gamma-secretase inhibitor). One cell line (MC3T3-E1) cells: four different experimental conditions: cultured with (1) control tumor cells + DMSO; (2) Jagged1-overexpressing tumor cells + DMSO; (3) control tumor cells + MRK-003; (4) Jagged1-overexpressing tumor cells + MRK-003. Each experiment has two biological replicates. Total, 8 samples.
2010-08-15 | E-GEOD-20517 | biostudies-arrayexpress
Project description:Transcriptional profiling of MC3T3-E1 osteoblasts that were flow cytometry-separated from cocultures with control or Jagged1-overexpressing tumor cells and treated with either DMSO control or 1μM MRK-003 (gamma-secretase inhibitor).
2010-08-15 | GSE20517 | GEO
Project description:Microarray study revealed 1324 genes that were up-regulated and 1550 genes that were down-regulated more than 1.5 fold change (corrected p<0.05) in MC3T3-E1-derived-mature Osteoblasts compared to control MC3T3-E1.
2019-04-21 | GSE46400 | GEO
Project description:In order to define the underlying mechanism of fluoride resistance in mammals and provide a theoretical basis for fluorosis treatment, high-throughput sequencing was applied to map the genetic changes of fluoride-resistant mouse osteoblasts. Fluoride-tolerant MC3T3-E1 cells were developed by gradient fluoride exposure. The differentially expressed genes of fluorine-resistant MC3T3-E1 cells were identified by high-throughput sequencing. High-throughput RNA sequencing identified 2702 differentially expressed genes (DEGs) showed more than 2-fold difference in 30ppm FR MC3T3-E1 cells, of which 17 DEGs were associated with ferroptosis.
2022-05-25 | GSE203511 | GEO
Project description:Osteoblasts are responsive to shear stress. We investigated the effect of of laminar fluid flow (LFF) on osteoblast-like MC3T3-E1 cells at two timepoints. We used microarray analysis to detail the global gene expression of MC3T3-E1 cells in response to 1 hour of laminar fluid flow directly and 4 hours after treatment.
2021-02-15 | GSE138160 | GEO
Project description:Caspase-9 is traditionally considered as the initiator caspase of the intrinsic apoptotic pathway. In the last decade, however, other functions beyond initiation/execution of cell death have been described including cell type-dependent regulation of proliferation, differentiation/maturation, mitochondrial and endosomal/lysosomal homeostasis. As previous studies revealed non-apoptotic functions of caspases in osteogenesis and bone homeostasis, this study was performed to identify proteins and pathways deregulated by knockout of caspase-9 in mouse MC3T3-E1 osteoblasts. Data-independent acquisition – parallel accumulation serial fragmentation (diaPASEF) proteomics was used to compare protein profiles of control and caspase-9 knockout cells. A total of 7669 protein groups were quantified and 283 upregulated/141 downregulated protein groups were associated with the caspase-9 knockout phenotype. The deregulated proteins were mainly enriched for those associated with cell migration/motility and DNA replication/repair. Altered migration was confirmed in MC3T3-E1 cells with genetic and pharmacological inhibition of caspase-9. ABHD2, an established regulator of cell migration, was identified as a possible substrate of caspase-9. We conclude that caspase-9 acts as a modulator of osteoblastic MC3T3-E1 cell migration and therefore may be involved in bone remodeling and fracture repair.
2024-04-17 | PXD045703 | Pride
Project description:Developing osteoblasts undergo a sequence of three consecutive phases: cell proliferation, extracellular matrix maturation, and mineralization. We investigated pH effects on these phases using the osteoblast-like cell line MC3T3-E1.
2016-12-28 | GSE84907 | GEO
Project description:Purpose: Identify PTH-responsive genes in MC3T3-E1 cells. The aim of the study is to identify novel gene targets that are reugulated by PTH signaling in bone, elicting its anabolic effect in osteoblasts. Methods: mRNA expression profiles were compared between Vehicle and PTH(1-34)-treated MC3T3-1 cells, in triplicates, using Illumina HiSeq 2000 PE100 sequncing. qPCR using Taqman probes were used to validate genes of interest. Results: Sequence reads per sample were mapped to the mouse genome (mm10) and differential expression of each gene was determined. Genes that showed differential expression between Vehicle vs PTH(1-34)-treated samples and has a relevant function in bone were further characterized by knockdown strategies in MC3T3-E1 cells. Conclusion: Our study have identified a list of novel genes regulated by PTH siganling. The characterization of their transcription and function in osteoblasts and osteocytes added to our knowledge of PTH signaling in bone and other skeletal tissues.
2020-07-14 | GSE154355 | GEO
Project description:Gene expression analysis of murine MC3T3-E1 cells induced to undergo synchronized osteoblastic differentiation in vitro. MC3T3-E1 cells were cultured in vitro for up to 28 days in the presence of 8-glycerol phosphate and ascorbic acid to induce osteoblastic differentiation. Total RNA was isolated after 2, 5, 10 and 28 days in culture to sample proliferating preosteoblasts (Day 2), growth arrested preosteoblasts (Day 5), differentiating osteoblasts (Day 10), and mature osteoblasts (Day 28). Timing of sample collection was based on direct measurements of cell number, alkaline phosphatase expression, type 1A collagen synthesis, and matrix mineralization in parallel cultures. Triplicate samples from each time point were hybridized to slide arrays printed with the Operon Mouse Oligo set, version 2.0.
2012-06-27 | E-GEOD-30393 | biostudies-arrayexpress
Project description:Breast cancer is one of the leading causes of cancer-related mortality in women. NOTCH signaling is a well conserved pathway which not only plays critical roles in normal development, but also in cancer progression. One of the Notch ligand, JAGGED1 is overexpressed in about 30% of breast cancer patients. However, the role of JAGGED1 in breast tumorigenesis has not been rigorously examined. By utilizing genetic engineered mouse models of mammary specific Jagged1 expression or knockout, we discover that Jagged1 promotes tumorigenesis in multiple spontaneous mammary tumor models. Jagged1 expression leads to increased infiltration of tumor associated macrophages and decreased presentation of T cells within tumor microenvironment. Depletion of macrophages or T cells by neutralizing antibodies diminishes the tumor-promoting effect caused by Jagged1. Mechanistically, Jagged1 activates Notch signaling in tumor cells, leads to increased expression and secretion of multiple cytokines, including IL-6 and WISP. These cytokines help recruit macrophages into the tumor microenvironment. Macrophages crosstalk with infiltrated T cells and inhibit their cytotoxic killing on tumor cells. In triple negative breast cancer patient samples, high expression level of JAGGED1 correlates with increased macrophage infiltration and decreased T cell infiltration within tumor tissues. JAGGED1 also promotes tumor progression in several other solid cancer types, including melanoma, and colon cancer in a T cell dependent manner. Co-administration of immune checkpoint inhibitor, PD-1 antibody with gamma-secretase inhibitor (GSI) significantly inhibits tumor growth. These findings identify a unique oncogenic crosstalk between tumor derived JAGGED1, Macrophages, and T cells to promote tumor progression.
2022-03-08 | GSE161769 | GEO