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Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis [RNA-Seq]

ABSTRACT: RNA-seq was performed on MG63.3-GFP cells in vitro or isolated from mouse lung 1 day or 22 days post-innoculation to assess gene expression dynamics during lung colonization.

ORGANISM(S): Homo sapiens

PROVIDER: GSE215757 | GEO | 2023/09/18

REPOSITORIES: GEO

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Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis [mg633_ATACseq]

Project description:ATAC-seq was performed on MG63.3-GFP cells in vitro or isolated from mouse lung 1 day or 22 days post-innoculation to assess chromatin accessbility dynamics during lung colonization.

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Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis [143b_ATACseq]

Project description:ATAC-seq was performed on 143b-GFP cells in vitro or isolated from mouse lung 1 day or 22 days post-innoculation to assess chromatin accessbility dynamics during lung colonization.

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Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis [scATAC-Seq]

Project description:Temporal profiling of chromatin accessibility during metastasis revealed dynamic changes in chromatin accessibility during osteosarcoma lung colonization. We sought to determine whether these changes were due to epigenomic reprogramming, or shifts in subclonal frequency. To do this we performed scATAC-seq on MG63.3-GFP cells grown in vitro.

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Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis

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

2023-09-15 | GSE215765 | GEO

Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis

Project description:Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis

| PRJNA890572 | ENA

Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis [mg633_ATACseq]

Project description:Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis [mg633_ATACseq]

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Project description:Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis [143b_ATACseq]

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Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis [RNA-Seq]

Project description:Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis [RNA-Seq]

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Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis [scATAC-Seq]

Project description:Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis [scATAC-Seq]

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Increased metastasis with loss of E2F2 in Myc-driven tumors

Project description:In human breast cancer, mortality is associated with metastasis to distant sites. Therefore, it is critical to elucidate the biological mechanisms that underlie tumor progression and metastasis. Using signaling pathway signatures we previously predicted a role for E2F transcription factors in Myc induced tumors. To test this role we interbred MMTV-Myc transgenic mice with E2F knockouts. Surprisingly, we observed that the loss of E2F2 sharply increased the percentage of lung metastasis in MMTV-Myc transgenic mice. Examining the gene expression profile from these tumors, we identified genetic components that were potentially involved in mediating metastasis. These genes were filtered to uncover the genes involved in metastasis that also impacted distant metastasis free survival in human breast cancer. In order to elucidate the mechanism by which E2F2 loss enhanced metastasis we generated knockdowns of E2F2 in MDA-MB-231 cells and observed increased migration in vitro and increased lung colonization in vivo. We then examined genes that were differentially regulated between tumors from MMTV-Myc, MMTV-Myc E2F2-/-, and lung metastases samples and identified PTPRD. To test the role of PTPRD in E2F2-mediated breast cancer metastasis, we generated a knockdown of PTPRD in MDA-MB-231 cells. We noted that decreased levels of PTPRD resulted in decreased migration in vitro and decreased lung colonization in vivo. Taken together, these data indicate that E2F2 loss results in increased metastasis in breast cancer, potentially functioning through a PTPRD dependent mechanism. Lung metastases from MMTV-Myc tumors in a E2F2 knockout and E2F3 +/- backgrounds were analyzed for their gene expression profile

2016-08-08 | E-GEOD-71815 | biostudies-arrayexpress

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