Establishment of an epithelioid malignant schwannoma cell line (YST-1)

Nagashima, Yoji; Ohaki, Yoshiharu; Tanaka, Yukichi; Sumino, Kaoru; Funabiki, Tetsunori; Okuyama, Toshiya; Watanabe, Shinichiro; Umeda, Makoto; Misugi, Kazuaki

doi:10.1007/bf02899420

Cited by 19 publications

(14 citation statements)

References 14 publications

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“…The fibroblasts were examined using antivimentin and anti-keratin antibodies, and were found to stain positively with anti-vimentin antibody but not with anti-keratin antibody. From the same subcutaneous tumor, a tumor cell line, MCAS-3S, was also re-established by the explant method described [25].…”

Section: Methodsmentioning

confidence: 99%

Marked induction of gelatinases, especially type B, in host fibroblasts by human ovarian cancer cells in athymic mice

et al. 1995

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Two human ovarian adenocarcinoma cell lines, MCAS-3 and OVISE-3 were found to secrete little of any type of gelatinase in tissue culture. However, when these cell lines were implanted subcutaneously into nude mice the cyst fluids from the resultant tumors contained gelatinase A and/or B. The enzyme activities, especially of gelatinase B, were much higher in the malignant MCAS-3 tumors than in those of the less malignant OVISE-3 tumor cells. To elucidate the origin of gelatinase B in cyst fluids of the MCAS-3 tumors, murine skin fibroblasts (MSF) were isolated from a subcutaneous tumor in a nude mouse and tested for their proteinase secretion in culture. MSF cells, which secreted some gelatinase A and gelatinase B, were induced to secrete high levels of both enzymes, especially gelatinase B, by co-cultivation with MCAS-3 cells. In addition, gelatinase A activity was induced by incubation of MSF cells with the conditioned medium of either MCAS-3 or OVISE-3 cells, whereas gelatinase B was induced only with that of MCAS-3. Although cytokines or growth factors such as IL-1 beta, TGF-beta 1, TNF-alpha or EGF stimulated the secretion of gelatinases A and B from MSF cells, their effects on gelatinase B activity were far less than that of the MCAS-3 conditioned medium. These results indicate that the major part of gelatinase B activity in the cyst fluids of the ovarian tumors is secreted by host interstitial cells stimulated by tumor-derived humoral factors. Similar tumor cell-host cell interactions may be important in the production of various proteinases in other tumor types.

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Section: Methodsmentioning

confidence: 99%

Marked induction of gelatinases, especially type B, in host fibroblasts by human ovarian cancer cells in athymic mice

et al. 1995

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“…NMS-2 and NMS-2PC cells were generously provided by Dr Akira Ogose (Department of Orthopedic Surgery, Niigata University, Niigata, Japan). The YST-1 cell line was derived from an epithelioid MPNST that occurred in the upper arm of an 8-year-old girl with no clinical evidence of NF1 (Nagashima et al, 1990). YST-1 cells were kindly provided by Dr Yoji Nagashima (Department of Pathology, Yokohama City University School of Medicine, Yokohama, Japan).…”

Section: Mpnst Cell Lines Neonatal Schwann Cells and Their Culture Cmentioning

confidence: 99%

Activation of the neuregulin-1/ErbB signaling pathway promotes the proliferation of neoplastic Schwann cells in human malignant peripheral nerve sheath tumors

et al. 2005

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Patients with neurofibromatosis type 1 develop aggressive Schwann cell neoplasms known as malignant peripheral nerve sheath tumors (MPNSTs). Although tumor suppressor gene mutations play an important role in MPNST pathogenesis, it is likely that dysregulated signaling by as yet unidentified growth factors also contributes to the formation of these sarcomas. To test the hypothesis that neuregulin-1 (NRG-1) growth factors promote mitogenesis in MPNSTs, we examined the expression and action of NRG-1 in human MPNSTs and neurofibromas, the benign precursor lesions from which MPNSTs arise. Multiple a and b transmembrane precursors from the class II and III NRG-1 subfamilies are present in both tumor types. Neoplastic Schwann cells within these neoplasms variably express the erbB kinases mediating NRG-1 responses (erbB2, erbB3 and/or erbB4). Human MPNST cell lines (Mash-1, YST-1, NMS-2 and NMS-2PC cells) similarly coexpress multiple NRG-1 isoforms and erbB receptors. These MPNST lines are NRG-1 responsive and demonstrate constitutive erbB phosphorylation. Treatment with PD168393 and PD158780, two structurally and mechanistically distinct erbB inhibitors, abolishes erbB phosphorylation and reduces DNA synthesis in these lines. These findings suggest that autocrine and/or paracrine NRG-1/erbB signaling promotes neoplastic Schwann cell proliferation and may be an important therapeutic target in neurofibromas and MPNSTs.

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“…A small number of cell lines, derived from NF1-associated MPNSTs (7-10) or sporadic MPNSTs (11,12), have been reported in the literature but have never been directly compared with each other and primary tumors. These cell lines are a valuable resource as primary MPNSTs are difficult to permanently establish in culture.…”

Section: Introductionmentioning

confidence: 99%

Large-Scale Molecular Comparison of Human Schwann Cells to Malignant Peripheral Nerve Sheath Tumor Cell Lines and Tissues

Miller¹,

Rangwala²,

Williams³

et al. 2006

Cancer Research

187

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Malignant peripheral nerve sheath tumors (MPNST) are highly invasive soft tissue sarcomas that arise within the peripheral nerve and frequently metastasize. To identify molecular events contributing to malignant transformation in peripheral nerve, we compared eight cell lines derived from MPNSTs and seven normal human Schwann cell samples. We found that MPNST lines are heterogeneous in their in vitro growth rates and exhibit diverse alterations in expression of pRb, p53, p14Arf , and p16INK4a proteins. All MPNST cell lines express the epidermal growth factor receptor and lack S100B protein. Global gene expression profiling using Affymetrix oligonucleotide microarrays identified a 159-gene molecular signature distinguishing MPNST cell lines from normal Schwann cells, which was validated in Affymetrix microarray data generated from 45 primary MPNSTs. Expression of Schwann cell differentiation markers (SOX10, CNP, PMP22, and NGFR) was downregulated in MPNSTs whereas neural crest stem cell markers, SOX9 and TWIST1, were overexpressed in MPNSTs. Previous studies have implicated TWIST1 in apoptosis inhibition, resistance to chemotherapy, and metastasis. Reducing TWIST1 expression in MPNST cells using small interfering RNA did not affect apoptosis or chemoresistance but inhibited cell chemotaxis. Our results highlight the use of gene expression profiling in identifying genes and molecular pathways that are potential biomarkers and/or therapeutic targets for treatment of MPNST and support the use of the MPNST cell lines as a primary analytic tool. (Cancer Res 2006; 66(5): 2584-91)

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Establishment of an epithelioid malignant schwannoma cell line (YST-1)

Cited by 19 publications

References 14 publications

Marked induction of gelatinases, especially type B, in host fibroblasts by human ovarian cancer cells in athymic mice

Marked induction of gelatinases, especially type B, in host fibroblasts by human ovarian cancer cells in athymic mice

Activation of the neuregulin-1/ErbB signaling pathway promotes the proliferation of neoplastic Schwann cells in human malignant peripheral nerve sheath tumors

Large-Scale Molecular Comparison of Human Schwann Cells to Malignant Peripheral Nerve Sheath Tumor Cell Lines and Tissues

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