Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA192552 | ENA |
REPOSITORIES: ENA
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2013-10-14 | E-GEOD-44936 | biostudies-arrayexpress
Project description:Transcriptional profiling of differential miRNA expression in mouse RAW264.7 preosteoclast cells comparing control untreated cells with RAW264.7 cells treated for 6 days. Treatment conditiones tested included 50ng/mL RANKL or indicated bone metastasis tumor cell conditioned media from 4T1, 4T1.2, TSU-PR1, and TSU-PR1-B2 cell lines.
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2014-02-06 | E-GEOD-48432 | biostudies-arrayexpress
Project description:This study aimed to elucidate the mechanism by which exosomes from bone-metastatic Lewis lung carcinoma (BM-LLC) cells promote osteolytic metastasis. We performed RNA-seq on mouse RAW264.7 macrophages (osteoclast precursors) treated with exosomes derived from either non-metastatic (NC-LLC) or bone-metastatic (BM-LLC) Lewis lung carcinoma cells. The goal was to identify differentially expressed genes and key regulatory pathways involved in exosome-induced osteoclast differentiation. Integrated analysis with small RNA sequencing data from the exosomes identified the miR-484-PECAM1 axis as a critical driver of this process. Our findings reveal that BM-LLC exosomes deliver miR-484 to recipient macrophages, repress PECAM1 expression, and subsequently upregulate osteoclastogenic markers (TRAP, CTSK, RANKL) and master transcription factors (NFATc1, c-Fos), thereby reprogramming osteoclastogenesis and driving bone destruction.
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Project description:A variety of genes are responsible for regulating osteoclastogenesis in response to RANK Ligand. Microarray analysis was used to identify genes sensitive to RANKL-induced osteoclastogenesis in RAW264.7 cells. RAW264.7 cells were incubated with 50 ng/mL RANKL or vehicle control (3 replicates each). After 48 h, total RNA were harvested by an RNeasy Plus Mini Kit (QIAGEN).
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Project description:We found that RANKL, expressed by cancer cells or derived from exogenous sources, consistently induced human prostate, breast, kidney, lung and liver cancer cells to colonize or metastasize to bone in an animal model of cancer bone metastasis. RANK-mediated signaling established a premetastatic niche through a forward feedback loop by inducing RANKL and c-Met expression and downstream signaling via upregulation of master regulator transcription factors regulating EMT (Twist1, Slug, Zeb1, Zeb2), stem cells (Sox2, Myc, Oct3/4 and Nanog), neuroendocrine cells (Sox 9, HIF-1α and FoxA2) and osteomimicry (c-Myc/Max, Sox2, Sox9, HIF1α and Runx2). Abrogating RANK or its downstream signaling network, c-Myc/Max or c-Met, abolished PCa skeletal metastasis in mice. We observed that a small number of RANKL-expressing PCa cells can initiate bone and soft tissue metastases by recruiting non-tumorigenic or bystander PCa or host cells from the circulation or at metastatic sites to co-colonize bone. The recruited bystander PCa cells assume the phenotypes of RANKL-expressing PCa cells by expressing increased c-Met, phosphorylated c-Met and RANKL. RANKL expression at a single cell level in primary PCa tissues predicted disease-specific survival, reflecting the significant role of RANKL-RANK signaling in the development of lethal bone metastasis.
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Project description:Transcriptional profiling of Candida albicans that had been phagocytosed for 1, 2, or 4 hours by either bone marrow-derived mouse macrophaged (BMDM) or immortalized RAW264.7 cells Keywords: Time course Two-condition experiment, phagocytosed cells vs cells maintained in D-10 media. Time course: 1, 2, and 4 hours. Biological replicates: 4 independent experiments at each cell-time combinations.
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