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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE207482 | GEO | 2023/08/02

REPOSITORIES: GEO

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

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PROM2 overexpression induces metastatic potential through epithelial-to-mesenchymal transition and ferroptosis resistance in human cancers.

Project description:IntroductionDespite considerable therapeutic advances in the last 20 years, metastatic cancers remain a major cause of death. We previously identified prominin-2 (PROM2) as a biomarker predictive of distant metastases and decreased survival, thus providing a promising bio-target. In this translational study, we set out to decipher the biological roles of PROM2 during the metastatic process and resistance to cell death, in particular for metastatic melanoma.Methods and resultsMethods and results: We demonstrated that PROM2 overexpression was closely linked to an increased metastatic potential through the increase of epithelial-to-mesenchymal transition (EMT) marker expression and ferroptosis resistance. This was also found in renal cell carcinoma and triple negative breast cancer patient-derived xenograft models. Using an oligonucleotide anti-sense anti-PROM2, we efficaciously decreased PROM2 expression and prevented metastases in melanoma xenografts. We also demonstrated that PROM2 was implicated in an aggravation loop, contributing to increase the metastatic burden both in murine metastatic models and in patients with metastatic melanoma. The metastatic burden is closely linked to PROM2 expression through the expression of EMT markers and ferroptosis cell death resistance in a deterioration loop.ConclusionOur results open the way for further studies using PROM2 as a bio-target in resort situations in human metastatic melanoma and also in other cancer types.

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