A biochemical and immunohistological study of collagen synthesis in Ewing's tumour

Harvey, W. Proctor; Squier, M. V.; Duance, Victor Colin; Pritchard, J A

doi:10.1038/bjc.1982.294

Cited by 11 publications

(2 citation statements)

References 14 publications

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“…Interestingly, in two different ES cell lines, derived from the same patients, a 2 b 1 was higher on primary cells compared with metastatic cells (vanValen et al, 1994). This may reflect the fact that the predominant collagen extracted from ES tissue and synthesized in short-term cultures is type I (Harvey et al, 1982). Therefore, cells lacking a 2 b 1 are less facilitated to have stable anchorage to the ECM in ES tissue and may have increased migratory abilities.…”

Section: Discussionmentioning

confidence: 92%

In Ewing's sarcoma CCN3(NOV) inhibits proliferation while promoting migration and invasion of the same cell type

et al. 2005

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Altered expression of CCN3 has been observed in a variety of musculoskeletal tumours, including Ewing's sarcoma (ES). Despite its widespread distribution, very little is known about its biological functions and molecular mechanisms of action. We transfected CCN3 gene into a CCN3-negative ES cell line and analysed the in vitro and in vivo behaviours of stably transfected clones. Forced expression of CCN3 significantly reduced cell proliferation in vitro, growth in anchorage-independent conditions, and tumorigenicity in nude mice. Despite the antiproliferative effect, CCN3-transfected ES cells displayed increased migration and invasion of Matrigel. The decreased expression of a2b1 integrin receptor and the increased amount of cell surface-associated matrix metalloproteinase (MMP)-9 following the expression of CCN3 may be the basis for the increased migratory abilities of transfected cells. Cells lacking a 2 b 1 are less facilitated to have stable anchorage since the predominant collagen extracted from ES tissue is indeed type I collagen, and proMMP-9 was recently found to provide a cellular switch between stationary and migratory ES cell phase. Our findings are in line with those recently obtained in glioblastoma. However, the underlying molecular mechanisms appear to be different, further highlighting the importance of the cellular context in the regulation of function of CCN proteins.

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Section: Discussionmentioning

confidence: 92%

In Ewing's sarcoma CCN3(NOV) inhibits proliferation while promoting migration and invasion of the same cell type

et al. 2005

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“…The contribution of ECM remodeling to growth and progression of EwS has not been deeply investigated, though clinico-pathologic correlative studies suggested that a stroma-rich TME influences EwS gene expression and patient prognosis (45). EwS cells and tumors can deposit fibrillar and non-fibrillar proteins (46)(47)(48) and we previously showed that activation of canonical Wnt/beta-catenin and TGF-beta signaling upregulates secretion of pro-tumorigenic andangiogenic matrisomal proteins by EwS cells, including collagens and TNC (49,50). In the current work, we have identified discrete subpopulations of EwS cells that deposit protumorigenic ECM proteins in vivo.…”

Section: Discussionmentioning

confidence: 99%

Carcinoma-associated fibroblast-like tumor cells remodel the Ewing sarcoma tumor microenvironment

Wrenn

Apfelbaum

Rudzinski

et al. 2023

Preprint

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Tumor heterogeneity is a major driver of cancer progression. In epithelial-derived malignancies, carcinoma-associated fibroblasts (CAFs) contribute to tumor heterogeneity by depositing extracellular matrix (ECM) proteins that dynamically remodel the tumor microenvironment (TME). Ewing sarcomas (EwS) are histologically monomorphous, mesenchyme-derived tumors that are devoid of CAFs. Here we identify a previously uncharacterized subpopulation of transcriptionally distinct EwS tumor cells that deposit pro-tumorigenic ECM. Single cell analyses revealed that these CAF-like cells differ from bulk EwS cells by their upregulation of a matrisome-rich gene signature that is normally repressed by EWS::FLI1, the oncogenic fusion transcription factor that underlies EwS pathogenesis. Further, our studies showed that ECM-depositing tumor cells express the cell surface marker CD73, allowing for their isolation ex vivo and detection in situ. Spatial profiling of tumor xenografts and patient biopsies demonstrated that CD73+ EwS cells and tumor cell-derived ECM are prevalent along tumor borders and invasive fronts. Importantly, despite loss of EWS::FLI1-mediated gene repression, CD73+ EwS cells retain expression of EWS::FLI1 and the fusion-activated gene signature, as well as tumorigenic and proliferative capacities. Thus, EwS tumor cells can be reprogrammed to adopt CAF-like properties and these transcriptionally and phenotypically distinct cell subpopulations contribute to tumor heterogeneity by remodeling the TME.

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Cell culture of small round cell tumor originating in the thoracopulmonary region. Evidence for derivation from a primitive pluripotent cell

Fujii

Hongo

Nakagawa

et al. 1989

Cancer

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The authors describe a 14-year-old girl with small round cell tumor originating in the chest wall analyzed by the extensive studies including light and electron microscopic examination, histochemical study, immunochemical study, cytogenetics, and gene analysis. A cell line producing carcinoembryonic antigen (CEA) and neuron-specific enolase (NSE) has been established from pleural effusion of the pulmonary metastatic tumor. Cytogenetic analysis disclosed a reciprocal translocation (11;22)(q24;q12). Additionally, immunocytochemical studies demonstrated that CEA, NSE, vimentin, cytokeratin, and epithelial membrane antigens are positive, but desmin and S-100 protein are negative. Although neurofilament was negative in the pulmonary metastatic tumor cells, it became positive in cell line in vitro. These results suggest that this tumor may be derived from the primitive and pluripotential cells, differentiating into mesenchymal, epithelial, and neural features in variable proportions.

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A biochemical and immunohistological study of collagen synthesis in Ewing's tumour

Cited by 11 publications

References 14 publications

In Ewing's sarcoma CCN3(NOV) inhibits proliferation while promoting migration and invasion of the same cell type

In Ewing's sarcoma CCN3(NOV) inhibits proliferation while promoting migration and invasion of the same cell type

Carcinoma-associated fibroblast-like tumor cells remodel the Ewing sarcoma tumor microenvironment

Cell culture of small round cell tumor originating in the thoracopulmonary region. Evidence for derivation from a primitive pluripotent cell

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