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Mouse polycomb group gene Cbx2 promotes osteoblastic but suppresses adipogenic differentiation in postnatal long bones

ABSTRACT: Mouse polycomb group gene Cbx2 promotes osteoblastic but suppresses adipogenic differentiation in postnatal long bones

PROVIDER: PRJNA445305 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6881030.fastq.gz	Fastqsanger.gz
	SRR6881031.fastq.gz	Fastqsanger.gz
	SRR6881032.fastq.gz	Fastqsanger.gz
	SRR6881027.fastq.gz	Fastqsanger.gz
	SRR6881028.fastq.gz	Fastqsanger.gz

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Mouse polycomb group gene Cbx2 promotes osteoblastic but suppresses adipogenic differentiation in postnatal long bones

Project description:A set of key developmental genes is essential for skeletal growth from multipotent progenitor cells at weaning. Polycomb group proteins, which regulate such genes contributes to the cell lineage commitment and subsequent differentiation via epigenetic chromatin modification and remodeling. However, it is unclear which cell lineage and gene sets are targeted by polycomb proteins during skeletal growth. We now report that mice deficient in a polycomb group gene Cbx2 (cterm/cterm) exhibited skeletal hypoplasia in the tibia, femur, and cranium. Long bone cavities in these mice contained fewer multipotent mesenchymal stromal cells. RNA-sequencing of bone marrow cells showed downregulation and upregulation of osteoblastic and adipogenic genes, respectively. Furthermore, the expression levels of genes specifically expressed in B-cell precursors were decreased. Forced expression of Cbx2 in Cbx2 (cterm/cterm) bone marrow stromal cell recovered fibroblastic colony formation and suppressed adipogenic differentiation. Collectively, our results suggest that Cbx2 controls the maintenance and adipogenic differentiation of mesenchymal stromal cells in the bone marrow.

2018-11-09 | GSE112227 | GEO

Transcriptomic analyses of the anti-adipogenic and pro-osteoblastic effects of aspirin in rat bone mesenchymal stem cell

Project description:Theoretically, the differentiation of mesenchymal stem cells (MSCs) into either adipocytic or osteoblastic phenotype can be deemed as a seesaw, where induction of one lineage comes at the expense of the other. Previously, researchers, including our team, found that aspirin promoted osteoblast differentiation of bone mesenchymal stem cells (BMSCs) whereas inhibiting adipogenic differentiation. However, the precise mechanisms, that is, which pathways, what biological process or key genes involved during this process, had not been systematically studied. In the present study, we tend to analyze the whole transcriptome of the anti-adipogenic and promote-osteoblastic effects of aspirin in BMSCs. Our results showed that aspirin’s presence restored or further strengthened the expression of an important part of the gene population repressed during adipogenesis or increased during osteogenesis. Besides, classical pathways related to osteogenic differentiation (p53 signaling pathway, focal adhesion, osteoclast differentiation, PI3K-Akt signaling pathway, MAPK signaling pathway, and Wnt signaling pathway) and the fat metabolism were also disturbed during the promote-osteoblastic and anti-adipogenic effects of aspirin. Therefore, our whole-genome transcriptomic results shed new light and open the door to more specific “omics” studies. Our results allow a better understanding of the anti-adipogenic and promote-osteoblastic effects of aspirin and pave the way to aspirin clinical use for the prevention and treatment of diseases like tissue defect and osteoporosis.

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Gene expression comparison of pre-osteoblastic and mature osteoblastic cell populations from 5 week old and 8 week old mice, a comparison of cell populations within and between age groups

Project description:The aim of the study was to identify gene expression profiles that distinguished different stages of osteoblast commitment, and determine whether the same osteoblast cell populations from mice of different ages had distinguishable expression profiles that may indicate functional changes are apparent for the cell populations during different stages of skeletal development. Pre-osteoblastic and mature osteoblastic cells were isolated from collagenase digested bones from 5 week old and 8 week wild type C57BL6 mice by FACS based on Lin, Sca-1, CD51, and CD31 cell surface markers.

2021-08-25 | GSE82285 | GEO

The HDAC inhibitor SAHA regulates CBX2 stability via a SUMO-triggered ubiquitin-mediated pathway in leukemia

Project description:Leukemias are characterized by bone marrow failure due to oncogenic mutations of hematopoietic stem cells (HSC) or blood precursor cells. HSC differentiation and self-renewal properties are tightly regulated by Polycomb group (PcG) proteins, a well-characterized family of transcriptional epigenetic regulators. PcG proteins form two canonical complexes: Polycomb repressive complex 1 (PRC1), and Polycomb repressive complex 2 (PRC2).CBX proteins link the activity of PRC1 with PRC2, serving as critical regulators of PcG-mediating activity. While the functional role of some CBX proteins in cancer has been largely explored, recent reports support the specific role of CBX2 in human tumors, thus it represent a promising new target for anti-cancer strategies. To date, chromodomain inhibitors have been identified for CBX7 , but no molecules inhibiting CBX2 have been described. Nevertheless, different chromatin-modulating drugs such as histone deacetylase inhibitors (HDACi) are reported to regulate CBX2 targets on chromatin, suggesting that HDACi might be used to indirectly modulate aberrant effects of CBX2 in cancer. We describe a novel SAHA-mediated mechanism of CBX2 post-translational regulation. We found that CBX2 undergoes SAHA-induced SUMO2/3 modification and that CBX2 SUMOylation promotes its ubiquitination and proteasome-dependent degradation. We also identified the specific molecular pathway and key players regulating CBX2 stability, demonstrating that CBX4 and RNF4 act as the E3 SUMO and E3 ubiquitin ligase, respectively. Additionally, CBX2-depleted leukemic cells display impaired proliferation, showing that CBX2 is required for leukemia cell clonogenicity. Our study provides the first evidence of a non-canonical SAHA-mediated anti-tumorigenic activity via CBX2 SUMOylation and degradation

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The molecular role of CBX2 in acute myeloid leukemia (AML)

Project description:The dynamic epigenome and proteins specialized in the interpretation of epigenetic marks critically contribute to leukemic pathogenesis but also offer opportunities for alternative therapeutic avenues. Targeting novel chromatin readers involved in leukemogenesis may thus provide new anticancer strategies. Accumulating evidence suggests that the PRC1 complex member CBX2 is overexpressed in solid tumors and promotes cancer cell survival. However, its role in leukemia is unclear. We found CBX2 overexpressed in leukemia both in vitro and ex vivo samples compared to CD34+ cells. Decreased CBX2 RNA levels prompted a robust reduction in cell proliferation and induction of apoptosis. Similarly, sensitivity to CBX2 silencing was observed in primary acute myeloid leukemia samples. CBX2 suppression also led to increased genome-wide chromatin accessibility followed by alteration of leukemic cell transcriptional programs, resulting in enrichment of cell death pathways and downregulation of survival genes. Intriguingly, CBX2 silencing induced epigenetic reprogramming at p38 MAPK-associated regulatory sites with consequent deregulation of gene expression. Our results identify CBX2 as a crucial player in leukemia progression and unveil a potential druggable CBX2-p38 MAPK route in AML.

2022-06-11 | GSE193477 | GEO

CBX2 knockdown in the PEO1 high grade serous cell line

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CBX2 overexpression in the OVCAR4 high grade serous cell line

2024-07-05 | GSE251945 | GEO

CBX2 Knockout in the OVCAR4 high grade serous cell line

2024-07-05 | GSE251944 | GEO

Fibroblasts under adipogenic, chondrogenic or osteogenic differentiation medium and controls

Project description:Global gene expression analysis was performed to investigate the changes of the fibroblast phenotype after four-week inductions toward adipocytic, osteoblastic and chondrocytic lineages. Human cells. Differential gene regulation, interpreted through Gene Set Enrichment Analysis, highlight important similarities and differences of induced fibroblasts compared to control cultures of human fibroblasts, adipocytes, osteoblasts and articular chondrocytes. Fibroblast controls were compared to Adipogenic induced fibroblasts and adipocytes. Gene sets were analysed with GSEA (webgestalt). Repeated for each lineage.

2012-03-01 | E-GEOD-35545 | biostudies-arrayexpress

The effect of CBX2 knockdown on gene expression in MCF-7 cells

Project description:To identify potential CBX2-regulated genes in ER positive cancer cells we assessed global gene expression changes in CBX2-depleted MCF-7 cells by RNA-sequencing analysis using the Illumina NovaSeq 6000 platform. Through Gene Set Enrichment Analysis we identified that CBX2 promotes cell growth, mTORC1 activation, E2F signalling.

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