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RKIP regulates bone homeostasis by mediating the differentiation fate of bone niche macrophages.

ABSTRACT: As central cells involved in osteoimmunology, bone niche macrophages possess diverse functions, and their differentiation fate regulates bone homeostasis. Elucidation of the underlying mechanism involved in macrophage differentiation is important for developing new therapeutic targets for osteoporosis. Our RNA-seq data showed that the differentially expressed genes in BMMs after RKIP knockout were involved in the pathways of cell adhesion and osteoclast differentiation.

ORGANISM(S): Mus musculus

PROVIDER: GSE264092 | GEO | 2024/05/01

REPOSITORIES: GEO

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RKIP regulates bone homeostasis by mediating the differentiation fate of bone niche macrophages.

Project description:RKIP regulates bone homeostasis by mediating the differentiation fate of bone niche macrophages.

| PRJNA1100972 | ENA

RKIP regulates differentiation-related features in melanocytic cells

Project description:Raf Kinase Inhibitor Protein (RKIP) has been extensively reported as an inhibitor of key signaling pathways involved in the aggressive tumor phenotype and shows decreased expression in several types of cancers. However, little is known about RKIP in melanoma or regarding its function in normal cells. We examined the role of RKIP in both primary melanocytes and malignant melanoma cells and evaluated its diagnostic and prognostic value. IHC analysis revealed a significantly higher expression of RKIP in nevi compared with early-stage (stage I-II, AJCC 8th) melanoma biopsies. Proliferation, wound healing, and collagen-coated transwell assays uncovered the implication of RKIP on the motility but not on the proliferative capacity of melanoma cells as RKIP protein levels were inversely correlated with the migration capacity of both primary and metastatic melanoma cells but did not alter other parameters. As shown by RNA sequencing, endogenous RKIP knockdown in primary melanocytes triggered the deregulation of cellular differentiation-related processes, including genes (i.e., ZEB1, THY-1) closely related to the EMT. Interestingly, NANOG was identified as a putative transcriptional regulator of many of the deregulated genes, and RKIP was able to decrease the activation of the NANOG promoter. As a whole, our data support the utility of RKIP as a diagnostic marker for early-stage melanomas. In addition, these findings indicate its participation in the maintenance of a differentiated state of melanocytic cells by modulating genes intimately linked to the cellular motility and explain the progressive decrease of RKIP often described in tumors.

2020-07-01 | GSE151585 | GEO

Inhibiting glutaminase exerts opposite effects on ovariectomy-induced and age-related reductions in murine bone mass

Project description:Recent studies have provided links between glutamine metabolism and bone remodeling, but little is known about its role in primary osteoporosis progression. We aimed to determine the effects of inhibiting glutaminase (GLS) on two types of primary osteoporosis and elucidate the related metabolism. To address this issue, age-related and ovariectomy (OVX)-induced bone loss mouse models were used to study the in vivo effects of CB-839, a potent and selective GLS inhibitor, on bone mass and bone turnover. We also studied the metabolic profile changes related with aging and GLS inhibition in primary bone marrow stromal cells (BMSC) and that related with OVX and GLS inhibition in primary bone marrow-derived monocytes (BMM). Besides, we studied the possible metabolic processes mediating GLS blockade effects during aging-impaired osteogenic differentiation and RANKL-induced osteoclast differentiation respectively via in vitro rescue experiments. We found that inhibiting GLS via CB-839 prevented OVX-induced bone loss while aggravated age-related bone loss. Further investigations showed that effects of CB-839 treatment on bone mass were associated with alterations of bone turnover. Moreover, CB-839 treatment altered metabolic profile in different orientations between BMSC of aged mice and BMM of ovariectomized mice. In addition, rescue experiments revealed that different metabolic processes mediated glutaminase blockade effects between aging-impaired osteogenic differentiation and RANKL-induced osteoclast differentiation. Taken together, our data demonstrated the different outcomes caused by CB-839 treatment between two types of osteoporosis in mice, which were tightly connected to the suppressive effects on both aging-impaired osteoblastogenesis and OVX-enhanced osteoclastogenesis mediated by different metabolic processes downstream of glutaminolysis.

2024-06-17 | MTBLS9415 | MetaboLights

Effect of knockdown of RKIP(=PEBP1) on gene expression in mouse breast cancer cells

Project description:Raf-1 kinase inhibitor protein (RKIP = PEBP1) has been shown to negatively regulate signaling pathways including the MAPK and NFkappaB pathways involved in cancer progression and metastasis. RKIP acts as a suppressor of metastasis, but the exact mechanisms are unclear. In this study, knockdown of RKIP expression was used to identify the targets of RKIP expression. GSEA analysis identified interferon response genes as downregulated in the RKIP knockdown cells.

2022-07-21 | GSE206259 | GEO

Gene expression data from THP-1 cells expressing RKIP shRNA vs control

Project description:Myeloid sarcoma (MS) is a subform of acute myeloid leukemia (AML), where myeloid blasts infilitrate extramedullary tissues, a process that resembles the formation of metastases in solid tumors. RKIP has been shown to be a metastasis-suppressor gene. Identification of genes modulated by RKIP in human AML cells helps us to identify mechanisms how RKIP could be involved in the formation of MS.

2018-01-01 | GSE103344 | GEO

Gene expression data from BM1 (1833) tumors that are wild type or overexpressing RKIP in a xenograft mouse model

Project description:RKIP is a metastasis suppressor that is lost or silenced in most metastatic cancers. Here we reintroduce RKIP exogenously into BM1 cells (bone-tropic derivative of MDA-MB-231 cells, also known as 1833) that lack RKIP expression, in order to study transcriptomic changes that lead to metastasis in vivo and identify actionable targets to be used in anti-metastatic treatment strategies.

2021-05-12 | GSE128983 | GEO

MicroRNA expression array for 1833 cells expressing RKIP vs. control

Project description:RKIP has been implicated in suppression of breast tumor metastasis. Identification of microRNAs regulated by RKIP helps us to understand how RKIP suppresses tumor metastasis via its downstream target mircoRNAs and genes. Total RNA was extracted from 1833 cells expressing RKIP or control, respectively. Exiqon miRCURY LNA array v.11.0. was performed to identify the microRNAs regulated by RKIP.

2014-07-01 | E-GEOD-47366 | biostudies-arrayexpress

Gene expression data from 1833 cells expressing RKIP vs control

Project description:RKIP regulates human breast tumor metastasis. We use gene expression array analysis to identify genes regulated by RKIP in human breast cancer cells. Total RNAs were extracted from 1833 cells expressing mutant RKIP (S153E-RKIP, a more potent Raf-1 inhibitor) and vector control. Affymetrix GeneChip hgu133plus2.0 Arrays were performed to detail the gene expression and identify the genes regulated by RKIP in human breast cancer cells.

2014-07-01 | E-GEOD-47378 | biostudies-arrayexpress

MicroRNA expression array for 1833 cells expressing RKIP vs. control

2014-07-01 | GSE47366 | GEO

Murine Bone Marrow Macrophages: Control vs. RANKL Stimulated

Project description:To identify the microRNAs that are involved in osteoclastogenesis, microRNA expression profiles in mouse bone marrow macrophages (BMMs) stimulated with RANKL (BMOc) were compared with that of control untreated BMMs. These results provide insights into the mechanisms to regulate osteoclastogenesis and bone resorption activities in osteoclasts by microRNA.

2013-07-10 | GSE48629 | GEO

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