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Role of Mcam in breast cancer cell state using a model cell line (Py230) [bulk RNA-Seq]

ABSTRACT: To investigate effect of Mcam KD on tumor gene expression profile in orthotopic Py230 derived grafted tumors

ORGANISM(S): Mus musculus

PROVIDER: GSE233090 | GEO | 2024/04/10

REPOSITORIES: GEO

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Role of Mcam in breast cancer cell state using a model cell line (Py230)

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

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Role of Mcam in breast cancer cell state using a model cell line (Py230) [single cell Multiplex]

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Cooperative polarization of MCAM/CD146 and ERM family proteins in melanoma

Project description:The WRAMP structure is a protein network associated with tail-end actomyosin contractility, membrane retraction, and directional persistence during cell migration. A marker of WRAMP structures is melanoma cell adhesion molecule (MCAM) which dynamically polarizes to the cell rear. However, factors that mediate MCAM polarization are still unknown. In this study, BioID using MCAM as bait identifies the ERM family proteins, moesin, ezrin, and radixin, as WRAMP structure components. We also present a novel image analysis pipeline, Protein Polarity by Percentile (“3P”), which classifies protein polarization using machine learning and facilitates quantitative analysis. Using 3P, we find that depletion of moesin, and to a lesser extent ezrin, decreases the proportion of cells with polarized MCAM. Furthermore, although co-polarized MCAM and ERM proteins show high spatial overlap, 3P identifies subpopulations with ERM proteins closer to the cell periphery. Live-cell imaging confirms that MCAM and ERM protein polarization is tightly coordinated, but ERM proteins enrich at the cell edge first. Finally, deletion of a juxtamembrane segment in MCAM previously shown to promote ERM protein interactions impedes MCAM polarization. Our findings highlight the requirement for ERM proteins in recruitment of MCAM to WRAMP structures and an advanced computational tool to characterize protein polarization.

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Circumventing Resistance within the Ewing Sarcoma Microenvironment by Anti-MCAM Chimeric Antigen Receptor Modified Ex-vivo Expanded Natural Killer Cells Combinatorial Therapy

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Project description:Ewing Sarcoma is the second most common solid pediatric malignant neoplasm of the bone and soft tissue. Driven by EWS/Ets, or rarely variant, oncogenic fusions, Ewing Sarcoma is a biologically and clinically aggressive disease with a high propensity for metastasis. Our laboratory has previously identified the Jumonji-domain H3K9 me 1/2 histone demethylase KDM3A as a novel oncogene downstream of EWS/Fli1, the most common oncofusion in Ewing Sarcoma. Herein, we uncover a role for KDM3A in the promotion of Ewing Sarcoma metastasis. Using global gene expression profiling, we show that some of the most strongly regulated genes by KDM3A are those implicated in cell migration and metastasis, and demonstrate, using functional assays, that KDM3A promotes migration in vitro and metastasis in vivo. We further provide evidence that MCAM, one of the most strongly and consistently regulated genes by KDM3A, is an important effector of KDM3A pro-metastatic action. Our studies also show that KDM3A regulates MCAM expression both through a direct mechanism, involving modulation of H3K9 methylation at the MCAM promoter, and an indirect mechanism, via the Ets1 transcription factor.

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