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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.

2023-09-18 | GSE215764 | GEO

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.

2023-09-18 | GSE215763 | GEO

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.

2023-09-18 | GSE215758 | GEO

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

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

Nidogen 1-enriched extracellular vesicles facilitate extrahepatic metastasis of liver cancer by activating pulmonary lung fibroblasts to secrete tumor necrosis factor receptor 1

Project description:In hepatocellular carcinoma (HCC) patients with extrahepatic metastasis, the lung is the most frequent site of metastasis. However, how the lung microenvironment favors disseminated cells remains unclear. Here, it is found that nidogen 1 (NID1) in HCC cell-derived EVs promoted pre-metastatic niche formation in the lung by enhancing angiogenesis and pulmonary endothelial permeability to facilitate colonization of cells and extrahepatic metastasis. Anti-NID1 antibody was able to block the lung colonization of tumor cells induced by HCC patient-derived EVs. EV-NID1 also activated fibroblasts, which secreted tumor necrosis factor receptor 1 (TNFR1), facilitated lung colonization of tumor cells and augmented HCC cell motility. In the clinical perspective, analysis of serum EV-NID1 and TNFR1 in HCC patients revealed their positive correlation and association with tumor stages suggesting the potential of these molecules as noninvasive biomarkers for the early detection of HCC. Administration of anti-TNFR1 antibody effectively diminished lung metastasis in mice. In conclusion, these results demonstrated the interplay of HCC EVs and activated fibroblasts in pre-metastatic niche formation and how blockage of their functions inhibits distant metastasis to the lungs. This study offers promise for the new direction of HCC treatment by targeting oncogenic EV components and their mediated pathways.

2020-11-17 | PXD019566 | Pride

The temporal progression of lung immune remodeling during breast cancer metastasis

Project description:The dynamics of immune reprogramming in the breast cancer lung metastastic niche remains incomplete. We used MULTI-seq (McGinnis, Patterson, et al., Nature Methods, 2019) to perform multiplexed single-cell RNA-sequencing analysis of cryopreserved lung immune cells isolated from PyMT mice, freshly-isolated lung immune cells isolated from PyMT mice, and cryopreserved lung immune cells isolated from 4T1 tumor-bearing mice from the onset of primary tumorigenesis through the formation of macrometastatic lesions. Cryopreserved PyMT samples were collected from 6-14 weeks of age, fresh PyMT samples were collected at 6, 10 and 13 weeks of age (with age-matched wild-type controls)

2024-04-22 | GSE263963 | GEO

Phenotypic states of leptomeningeal metastasis

Project description:Leptomeningeal metastasis (LM), or spread of cancer cells into the cerebrospinal fluid, is characterized by a rapid onset of debilitating neurological symptoms and markedly bleak prognosis. The lack of reproducible in vitro and in vivo models has prevented development of novel, LM-specific therapies. Although LM allows for longitudinal sampling of floating cancer cells with a spinal tap, attempts to culture patient-derived leptomeningeal cancer cells have not been successful. We therefore employ leptomeningeal derivatives of human breast and lung cancer cell lines that reproduce both floating and adherent phenotypes of human LM in vivo and in vitro. We introduce a trypsin/EDTA-based fractionation method to reliably separate the two cell subsets and demonstrate that in vitro cultured floating cells have decreased proliferation rate, lower ATP content, and are enriched in distinct metabolic signatures. Long-term fractionation and transcriptomic analysis suggest a high degree plasticity between the two phenotypes in vitro. Floating cells colonize mouse leptomeninges more rapidly and associate with shortened survival. In addition, patients harboring LM diagnosed with CSF disease alone succumbed to the disease earlier than patients with adherent (MRI-positive) disease. Together, these data support mechanistic evidence of a metabolic adaptation that allows cancer cells to thrive in their natural environment but leads to death in vitro.

2020-01-21 | GSE137020 | GEO

Osteosarcoma cells-derived secretome induce pre-metastatic changes in the lung microenvironment that support lung metastasis formation

Project description:To investigate the molecular and cellular alterations occurring in the lung tissue during the pre-metastatic niche formation in osteosarcoma, we used two two experimental mouse models and a multi-omics approach.

2024-01-26 | PXD040814 | Pride

MicroRNA-mRNA networks define translatable molecular outcome phenotypes in osteosarcoma.

Project description:There is a lack of well validated prognostic biomarkers in osteosarcoma, a rare, recalcitrant disease for which treatment standards have not changed in over 20 years. We performed microRNA sequencing in 74 frozen osteosarcoma biopsy samples, constituting the largest single center translationally analyzed osteosarcoma cohort to date, and we separately analyzed a multi-omic dataset from a large NCI supported national cooperative group cohort. We validated the prognostic value of candidate microRNA signatures and contextualized them in relevant transcriptomic and epigenomic networks. Our results reveal the existence of molecularly defined phenotypes associated with outcome independent of clinicopathologic features. Through machine learning based integrative pharmacogenomic analysis, the microRNA biomarkers identify novel therapeutics for stratified application in osteosarcoma. The previously unrecognized osteosarcoma subtypes with distinct clinical courses and response to therapy could be translatable for discerning patients appropriate for more intensified, less intensified, or alternate therapeutic regimens.

| S-EPMC7064533 | biostudies-literature

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