Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

AnxA1 inhibits pathological bone resorption

ABSTRACT: We explored the functional role of AnxA1 in osteoclastogenesis and pathological bone loss associated with inflammatory osteolysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE183145 | GEO | 2022/05/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

AnxA1 inhibits pathological bone resorption

Project description:AnxA1 inhibits pathological bone resorption

| PRJNA759264 | ENA

miRNA expression data from MCF-7 cells, overexpressing ANXA1

Project description:Annexin 1 (ANXA1), an endogenous anti-inflammatory protein which modulates cellular processes such as proliferation, differentiation and apoptosis has been implicated in cancer initiation and progression. ANXA1 was previously shown to be regulated by hsa-miR-196a and promoted cell proliferation and anchorarge-dependent growth and suppressed apoptosis. However, whether ANXA1 itself regulates miRNA expression is unknown. Therefore, in this study, we investigated the regulation of miRNA by ANXA1 in breast cancer cells. Using microarray technology, 12 miRNAs were found to be significantly and consistently downregulated in MCF-7 cells (MCF-V5) overexpressing ANXA1 overexpressing MCF-7 cells (MCF-V5). Hsa-miR-26b* and hsa-miR-562 were chosen for further investigation.The data suggest that miR-26b* and miR-562 may play a role in ANXA1-induced migration and possibly angiogenesis by targeting NFKB and point towards a potential therapeutic target for breast cancer. Breast cancer MCF-7 cells (MCF-V5) overexpressing ANXA1 were cultured for RNA extraction and hybridization on Affymetrix miRNA microarrays. These were compared against the control, which were MCF-7 cells (MCF-EV) carrying an empty expression vector. Expression analyses were carried out in triplicates

2015-01-05 | E-GEOD-54439 | biostudies-arrayexpress

miRNA expression data from MCF-7 cells, overexpressing ANXA1

2015-01-05 | GSE54439 | GEO

Absence of Anxa1 in myeloid lineage cells exacerbates acute pancreatitis (AP)

Project description:To elucidate the role of macrophage Anxa1 in the pathogenesis of AP, we intercrossed Anxa1flox/flox (Anxa1f/f or Anxa1 WT, as control) with Lyz2-Cre mice to create myeloid-specific Anxa1-knockout (Anxa1CKO) mice. We induced AP with repeated injection of cerulein in Anxa1CKO and Anxa1f/f littermates and examined the pancreas injury and inflammation. Pancreas tissue samples were collected at 12 hours after the first cerulein injection and performed RNA-seq.

2023-12-15 | GSE249714 | GEO

Inhibition of DOT1L increases osteoclast fusion and resorption and aggravates bone loss

Project description:Osteoclasts are absorptive cells and play a critical role in homeostatic bone remodeling and pathological bone resorption. Emerging evidence suggests an important role for epigenetic regulation of osteoclastogenesis. In this study, we investigated the role of DOT1L, which regulates gene expression epigenetically by histone H3K79 methylation during osteoclast formation. DOT1L and H3K79me2 levels were upregulated during osteoclast differentiation. Small molecule inhibitor- (EPZ5676 or EPZ004777) or short hairpin RNA-mediated reduction in DOT1L expression promoted osteoclast differentiation and resorption. DOT1L inhibition also increased osteoclast area and accelerated bone mass reduction in a mouse ovariectomy (OVX) model of osteoporosis. DOT1L inhibitors did not alter osteoblast differentiation in vitro and in vivo. Proteomics data, together with bioinformatics analysis, revealed that DOT1L inhibition altered reactive oxygen species (ROS) generation, autophagy activation, and cell fusion-related protein expression. ROS generation increased, and autophagy activation and cell migration ability enhancement were verified subsequently by flow cytometry and transwell migration assays. DOT1L inhibition increased NFATc1 nuclear translocation and NF-κB activation and strengthend osteoclast fusion and expression of resorption-related protein CD9, and MMP9 in osteoclasts derived from RAW264.7. Our findings support a new mechanism of DOT1L-mediated H3K79me2 epigenetic regulation of osteoclast differentiation, implicating DOT1L as a new therapeutic target for osteoclast dysregulation-induced disease.

2018-01-24 | PXD006448 | Pride

ANXA1 promotes cell proliferation and drug-resistance in B cell acute lymphoblastic leukemia

Project description:ANXA1 promoted cell proliferation, suppressed cell apoptosis induced cell cycle arrest in B-ALL cells by CCK8, Flow cytometry and RNA-seq Sequencing analysis. The in vivo results indicated that down-regulation of ANXA1 in B-ALL cells could significantly reduce leukemic cell burden. We then performed gene expression profiling using data obtained from RNA-seq of B-ALL cells with the ANXA1 gene down-regulated in CCRF-SB.

2024-02-01 | GSE226449 | GEO

The cell-intrinsic role of ANXA1 in human ILC2s

Project description:To investigate the effect of ANXA1, encoding annexin a1, on group 2 innate lymphoid cells (ILC2s), we downregulated the expression using lentiviral vector-based shRNA transfer and performed RNA-seq analysis.

2023-09-01 | GSE212517 | GEO