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RANK is an independent biomarker of poor prognosis in estrogen receptor-negative breast cancer and functionally contributes to increase tumor aggressiveness

ABSTRACT: RANK is an independent biomarker of poor prognosis in estrogen receptor-negative breast cancer and functionally contributes to increase tumor aggressiveness

PROVIDER: PRJNA769401 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16233400.fastq.gz	Fastqsanger.gz
	SRR16233401.fastq.gz	Fastqsanger.gz
	SRR16233402.fastq.gz	Fastqsanger.gz
	SRR16233403.fastq.gz	Fastqsanger.gz
	SRR16233404.fastq.gz	Fastqsanger.gz

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RANK is an independent biomarker of poor prognosis in estrogen receptor-negative breast cancer and functionally contributes to increase tumor aggressiveness

Project description:Analyses of genes expression in estrogen receptor negative, RANK positive, breast cancer orthoxenografts after in vivo treatment (4 weeks) with RANKL , RANK-Fc or denosumab.

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Rank pathway activation attenuates mammary tumorigenesis by inducing senescence

Project description:Rank overexpression attenuates mammary tumorigenesis by inducing senescence in mammary epithelial cells but enhances tumor aggressiveness by increasing stemness.

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Disruption of basal cell identity by Rank signaling drives mammary tumorigenesis

Project description:Rank signaling regulates mammary gland development and epithelial cell differentiation. Rank receptor is expressed by mammary basal and luminal populations, but, unlike luminal Rank, the contribution of basal Rank signaling to MG homeostasis remains poorly studied. We have combined timely regulated basal specific Rank expression with lineage tracing models and unveiled that basal Rank signaling controls basal cell identity in postnatal mammary glands. Ectopic basal Rank disrupts basal but also luminal cell identity, resulting in aberrant luminal-like differentiation of basal cells and impaired lactogenesis. Mechanistically, overactivation of basal Rank signaling leads to basal cell lineage infidelity, illustrated by the appearance of premalignant lesions composed by a basal-derived hybrid population with alveolar features which ultimately generates basal and luminal breast adenocarcinomas. Proteomic, transcriptomic and chromatin analyses support that the loss of tumor suppressive epigenetic regulators driven by basal Rank contributes to epithelial cell dedifferentiation and tumorigenesis. The basal Rank signature generated associates to poor prognosis particularly in human adenocarcinomas of the luminal subtype stressing the clinical relevance of our findings. Interestingly, our results reinforce the idea that luminal breast tumors might originate from basal cells that have suffered a luminal-like aberrant dedifferentiation triggered by Rank signaling.

2026-02-02 | PXD054102 | Pride

Rank signaling drives basal cell-lineage infidelity leading to mammary tumorigenesis

Project description:Rank signaling regulates mammary gland development and epithelial cell differentiation. Rank receptor is expressed by mammary basal and luminal populations, but unlike that of luminal, the contribution of basal Rank signaling to mammary gland homeostasis remains poorly studied. Combining timely-regulated, basal-specific Rank expression with lineage tracing strategies we unveiled that Rank signaling controls basal cell identity in postnatal mammary glands. Enhanced basal Rank disrupts basal and luminal cell identity, resulting in aberrant luminal-like differentiation of basal cells, defective lactation and the appearance of premalignant lesions composed of a basal-derived hybrid population with luminal/alveolar features, which ultimately generates basal and luminal breast adenocarcinomas. Mechanistically, phospho-proteomic, transcriptomic and chromatin analyses support that basal Rank activation triggers the loss of tumor suppressive epigenetic regulators, leading to chromatin remodeling, disruption of basal identity and tumorigenesis. We uncover a basal Rank gene signature that can be predictive of progression from in situ to invasive adenocarcinomas and associates with poor prognosis in breast cancer patients, particularly in those diagnosed with luminal adenocarcinomas, underlining the clinical relevance of our findings. Our results reinforce the idea that basal lineage infidelity triggered by Rank signaling contribute to generation from pre-invasive lesions and transition to invasive breast cancer.

2026-02-02 | PXD058134 | Pride

CD45- sorted tumor cells from RANK+/+ and RANK-/- MMTV_PYMT late carcinomas

Project description:Transcriptional profile of either RANK+/+ or RANK-/- MMTV-PyMT late carcinomas, orthotopically injected in syngeneic RANK+/+ mice. Once host mice developed tumors, CD45- tumor cells were sorted by flow cytometry in order to compare changes on tumor gene expression caused by the absence of RANK protein.

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Disruption of basal cell identity by Rank signaling drives mammary tumorigenesis

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Disruption of basal cell identity by Rank signaling drives mammary tumorigenesis

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CD45- sorted tumor cells from RANK+/+ and RANK-/- MMTV_PYMT late carcinomas

Project description:CD45- sorted tumor cells from RANK+/+ and RANK-/- MMTV_PYMT late carcinomas

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Transcriptome analysis of RANK-positive and RANK-negative luminal progenitor subpopulations in the human breast

Project description:RANK-positive and RANK-negative luminal progenitor cells were isolated by FACS from histologically normal human breast tissue from wild-type human donors. RNA-seq gene expression profiling was used to find differentially expressed genes between the RANK-positive and RANK-negative cell populations.

2016-06-20 | GSE71203 | GEO

Multiple myeloma immunoglobulin lambda translocations portend poor prognosis

Project description:Multiple myeloma immunoglobulin lambda translocations portend poor prognosis

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