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Impact of the bone microenvironment on phenotypic plasticity of ER+ breast cancer cells

ABSTRACT: Impact of the bone microenvironment on phenotypic plasticity of ER+ breast cancer cells

PROVIDER: PRJNA673695 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10096920_1.fastq.gz	Fastqsanger.gz
	SRR10096920_2.fastq.gz	Fastqsanger.gz
	SRR10096921_1.fastq.gz	Fastqsanger.gz
	SRR10096921_2.fastq.gz	Fastqsanger.gz
	SRR10096922_1.fastq.gz	Fastqsanger.gz

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Impact of the bone microenvironment on phenotypic plasticity of ER+ breast cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

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The bone microenvironment increases phenotypic plasticity of ER<sup>+</sup> breast cancer cells.

Project description:Estrogen receptor-positive (ER+) breast cancer exhibits a strong bone tropism in metastasis. How the bone microenvironment (BME) impacts ER signaling and endocrine therapy remains poorly understood. Here, we discover that the osteogenic niche transiently and reversibly reduces ER expression and activities specifically in bone micrometastases (BMMs), leading to endocrine resistance. As BMMs progress, the ER reduction and endocrine resistance may partially recover in cancer cells away from the osteogenic niche, creating phenotypic heterogeneity in macrometastases. Using multiple approaches, including an evolving barcoding strategy, we demonstrated that this process is independent of clonal selection, and represents an EZH2-mediated epigenomic reprogramming. EZH2 drives ER+ BMMs toward a basal and stem-like state. EZH2 inhibition reverses endocrine resistance. These data exemplify how epigenomic adaptation to BME promotes phenotypic plasticity of metastatic seeds, fosters intra-metastatic heterogeneity, and alters therapeutic responses. Our study provides insights into the clinical enigma of ER+ metastatic recurrences despite endocrine therapies.

| S-EPMC8062036 | biostudies-literature

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