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RNASeq of bone lining niche cell components from healthy vs. myeloma-bearing mice

ABSTRACT: RNASeq of bone lining niche cell components from healthy vs. myeloma-bearing mice

PROVIDER: PRJNA559729 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9947480.fastq.gz	Fastqsanger.gz
	SRR9947490.fastq.gz	Fastqsanger.gz
	SRR9947500.fastq.gz	Fastqsanger.gz
	SRR9947510.fastq.gz	Fastqsanger.gz
	SRR9947481.fastq.gz	Fastqsanger.gz

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RNASeq of bone lining niche cell components from healthy vs. myeloma-bearing mice

Project description:We compare gene expression in FACS-sorted bone-lining cell components: stromal progenitors, osteoprogenitors and endothelial cells, from myeloma-bearing vs. from healthy mice, and also between myeloma cells flushed from the central bone marrow vs. myeloma cells digested from the bone surface (myeloma-bearing mice only). The myeloma model used is the 5TGM1 murine myeloma cell line, injected into immunocompetent KaLwRij mice.

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RNASeq of bone lining niche cell components from myeloma-bearing mice treated daily with small molecule LDN193189 (LDN) or vehicle control

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Osteoclasts Control Re-activation of Dormant Myeloma Cells by Remodeling the Endosteal Niche

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Niche modulated versus niche modulating genes in multiple myeloma

Project description:Background. Multiple myeloma (MM) cells depend on the bone marrow (BM) niche for growth and survival. However, the tumor genes regulated by the niche are largely unknown. Design and Methods. BM aspiration samples were obtained from MM-patients with a high tumor load. Gene expression profile (GEP) was recorded immediately following aspiration and at subsequent time points. Identification of niche-regulated genes relied on spontaneous gene modulation following loss of niche regulation. Results. Compared to the reference samples fixed immediately following aspiration, the BM samples fixed after longer delay acquired numerous changes in GEP. The top modulated genes included a common subset of ~ 60 genes displaying prompt and sustained “switch” in expression consistently, among which were oncogenes (FOS, JUN) and genes regulating homing (CD69, RGS1), expansion and angiogenesis (AREG, PTGS2, RGS2, NR4A2). Interestingly, the “switch” in GEP was reversible and turned “off” and “on” in culture conditions resuming cell-cell-matrix contact versus re-spread into suspension, respectively. Moreover, the resuming of contact prolonged the survival of the tumor cells out-of-niche and the regression of the “contactless switch” was followed by induction of a new set of genes this time mostly encoding extracellular proteins, including angiogenic factors (IL8, CXCL5), extracellular-matrix proteins (SPP1, FN1), chemokines (CXCL5, CCL2, CCL20) and growth factors (CCL2, IL6). Conclusions. Our dataset, being unique in authentic expression design, uncovered contact-regulated genes capable of controlling homing, expansion and tumorigenesis. The adaptive response of the tumor cells to culture conditions deficient of integral niche components (e.g., vascular vessels) uncovered inducible niche-regulating tumor genes.

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