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Eribulin induces mesenchymal-epithelial transition to curtail metastatic progression by altering the chromatin landscape of breast cancers cells [scRNA-Seq]

ABSTRACT: Eribulin induces mesenchymal-epithelial transition to curtail metastatic progression by altering the chromatin landscape of breast cancers cells [scRNA-Seq]

PROVIDER: PRJNA856793 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20026300.fastq.gz	Fastqsanger.gz
	SRR20026301.fastq.gz	Fastqsanger.gz
	SRR20026302.fastq.gz	Fastqsanger.gz
	SRR20026303.fastq.gz	Fastqsanger.gz
	SRR20026304_1.fastq.gz	Fastqsanger.gz

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Eribulin induces mesenchymal-epithelial transition to curtail metastatic progression by altering the chromatin landscape of breast cancers cells

Project description:Eribulin induces mesenchymal-epithelial transition to curtail metastatic progression by altering the chromatin landscape of breast cancers cells

| PRJNA856790 | ENA

Eribulin induces mesenchymal-epithelial transition to curtail metastatic progression by altering the chromatin landscape of breast cancers cells [scATAC-Seq]

Project description:Eribulin induces mesenchymal-epithelial transition to curtail metastatic progression by altering the chromatin landscape of breast cancers cells [scATAC-Seq]

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Eribulin induces mesenchymal-epithelial transition to curtail metastatic progression by altering the chromatin landscape of breast cancers cells [scRNA-Seq]

Project description:The epithelial-mesenchymal transition (EMT) is a developmental program that is co-opted by tumor cells to aid in their embarking on the metastatic cascade. Tumor cells that undergo EMT are known to be endowed by, amongst other traits, heightened resistance to chemotherapy. Despite a clear understanding of the role played by the EMT program in conferring cells with these aggressive traits, there are currently no therapeutic avenues specifically targeting the program. Here we show that treatment of mesenchymal-like breast cancer cells with eribulin, an FDA-approved drug for the treatment of advanced breast cancers, leads to a mesenchymal-epithelial transition (MET), accompanied by a loss of metastatic propensity and sensitization of tumor cells to subsequent rounds of chemotherapy. We uncover a novel alternate mechanism of action that provides evidence for eribulin pretreatment as a viable clinical mechanism of MET induction that curtails metastatic progression and the evolution of therapy resistance.

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Eribulin induces mesenchymal-epithelial transition to curtail metastatic progression by altering the chromatin landscape of breast cancers cells [scATAC-Seq]

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Eribulin induces mesenchymal-epithelial transition to curtail metastatic progression by altering the chromatin landscape of breast cancers cells

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

2023-08-02 | GSE207482 | GEO

Alteration of DNMT1/DNMT3A by eribulin elicits global DNA methylation changes with potential therapeutic implications for triple-negative breast cancer

Project description:Triple-negative breast cancer (TNBC) is an aggressive disease subtype with limited treatment options. Eribulin is a chemotherapeutic approved for the treatment of advanced breast cancer that has been shown to elicit epigenetic changes. We investigated the effect of eribulin treatment on genome-scale DNA methylation patterns in TNBC cells. Following repeated treatment, The results showed that eribulin-induced changes in DNA methylation patterns evident in persister cells. Eribulin also affected the binding of transcription factors to genomic ZEB1 binding sites and regulated several cellular pathways, including ERBB and VEGF signaling and cell adhesion. Eribulin also altered the expression of epigenetic modifiers including DNMT1, TET1, and DNMT3A/B in persister cells. Data from primary human TNBC tumors supported these findings: DNMT1 and DNMT3A levels were altered by eribulin treatment in human primary TNBC tumors. Our results suggest that eribulin modulates DNA methylation patterns in TNBC cells by altering the expression of epigenetic modifiers. These findings have clinical implications for using eribulin as a therapeutic agent.

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Breast cancer cell lines treated with eribulin and paclitaxel

Project description:Eribulin mesylate is a synthetic macrocyclic ketone analog of the marine sponge natural product halichondrin B. Eribulin is a mechanistically unique inhibitor of microtubule dynamics, leading to inhibition of microtubule growth in the absence of effects on microtubule shortening at microtubule plus ends, and formation of nonproductive tubulin aggregates. In this study, we investigated whether selective signal pathways were associated with eribulin activity compared to paclitaxel, which stabilizes microtubules, based on gene expression profiling of cell line panels of breast, endometrial, and ovarian cancer in vitro. 27 breast cancer cell lines treated with eribulin and paclitaxel for 24 hours at concentration 10xIC50. Three technical replicates were included. for eribulin , paclitaxel and untreated cell lines.

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Endometrial cancer cell lines treated with eribulin and paclitaxel

Project description:Eribulin mesylate is a synthetic macrocyclic ketone analog of the marine sponge natural product halichondrin B. Eribulin is a mechanistically unique inhibitor of microtubule dynamics, leading to inhibition of microtubule growth in the absence of effects on microtubule shortening at microtubule plus ends, and formation of nonproductive tubulin aggregates. In this study, we investigated whether selective signal pathways were associated with eribulin activity compared to paclitaxel, which stabilizes microtubules, based on gene expression profiling of cell line panels of breast, endometrial, and ovarian cancer in vitro. 19 endometrial cancer cell lines treated with eribulin and paclitaxel for 24 hours at concentration 10xIC50. Three technical replicates were included. for eribulin , paclitaxel and untreated cell lines.

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Ovarian cancer cell lines treated with eribulin and paclitaxel

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Therapeutic induction of mesenchymal-epithelial transition via epigenetic reprogramming curtails metastatic progression and sensitizes breast cancers to treatment [RNA-seq]

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