Oncostatin M Is a Growth Factor for Ewing Sarcoma

David, Emmanuelle; Tirode, Franck; Baud’huin, Marc; Guihard, Pierre; Laud, Karine; Delattre, Olivier; Heymann, Marie Françoise; Heymann, Dominique; Rédini, Françoise; Blanchard, Frédéric

doi:10.1016/j.ajpath.2012.07.023

Cited by 37 publications

(32 citation statements)

References 54 publications

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“…Immunostaining was performed as described previously19 20 with the following primary antibodies: goat anti-ionized calcium-binding adapter molecule 1 (Iba1; Abcam, Cambridge, UK), goat anti-CD3 (Abcam), rat anti-CD45R (BD Biosciences, San Jose, California, USA) rat anti-Ly6G (Abcam).…”

Section: Methodsmentioning

confidence: 99%

IL-38 overexpression induces anti-inflammatory effects in mice arthritis models and in human macrophages in vitro

et al. 2017

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Section: Methodsmentioning

confidence: 99%

IL-38 overexpression induces anti-inflammatory effects in mice arthritis models and in human macrophages in vitro

et al. 2017

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“…It has been reported previously that OSM can promote IL-6, STAT3 induction and increase c-Myc expression [9,12,13]. We therefore examined levels of each of these in HCK1T cells overexpressing HPV16E6 (Dox ?…”

Section: The Effect Of Osm Induced By Hpv16e6 On Il-6 Stat3 and C-mycmentioning

confidence: 98%

Effect of human papillomavirus 16 oncoproteins on oncostatin M upregulation in oral squamous cell carcinoma

et al. 2016

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Human papillomavirus (HPV) infection modulates several host cytokines contributing to cancer development. Oncostatin M (OSM), an IL-6 family cytokine, acts to promote cell senescence and inhibit growth. Its dysregulation promotes cell survival, cell proliferation and metastasis in various malignancies. The effect of HPV on OSM dysregulation has not been investigated. To elucidate this, immunohistochemistry was used on formalin-fixed, paraffin-embedded oral squamous cell carcinoma (OSCC) tissues: HPV-positive (50) and HPV-negative (50) cases. Immortalized human cervical keratinocytes expressing HPV16E6 (HCK1T, Tet-On system) were used to demonstrate the role of HPV16E6 in OSM expression. In addition, a vector containing HPV16E6/E7 was transiently transfected into oral cancer cell lines. Cell viability, cell-cycle progression and cell migration were evaluated using flow cytometry and a wound healing assay, respectively. The results showed various intensities of OSM expression in OSCC. Interestingly, the median percentages of strongly stained cells were significantly higher in HPV-positive OSCCs than in HPV-negative OSCCs. To explore the role of HPV oncoproteins on OSM expression, the expression of HPV16E6 in the HCK1T Tet-On condition was induced by doxycycline and HPV16E6 was found to significantly upregulate levels of OSM mRNA and protein, with concomitant upregulation of c-Myc. In addition, the levels of OSM mRNA and protein in E6/E7 transiently transfected oral cancer cells also gradually increased in a time-dependent manner and these transfected cells showed greater viability and higher migration rates and cell-cycle progression than controls. This result demonstrates that HPV16 oncoproteins upregulate OSM and play an important role to promote OSCC development.

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“…29,30 CH03 cells were also injected together with 1 Â 10 6 human mesenchymal stem cells into the paratibial muscle as described. 29 Radiographs of subcutaneous or paratibial tumors were obtained with an MX-20 Digital Radiography System (Faxitron Bioptics, LLC, Tucson, AZ, USA).…”

Section: Tumorigenicity In Nude Micementioning

confidence: 99%

“…30 For human MSCs, 10 ml of bone marrow was harvested by iliac crest aspiration from a 39-year-old male donor (after informed consent and ethical approval). MSCs were obtained as previously described 31 and cultured in a medium composed of MEM-a (Gibco Life-Technologies), 1% P/S, 10% FBS, 1 ng/ml basic fibroblast growth factor (bFGF; R&D systems, Minneapolis, MN, USA) and 2 mM L-glutamine.…”

Section: Other Cells and Culture Conditionsmentioning

confidence: 99%

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New chondrosarcoma cell lines and mouse models to study the link between chondrogenesis and chemoresistance

Monderer

Luseau²,

Bellec

et al. 2013

Laboratory Investigation

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Chondrosarcomas are cartilage-forming, poorly vascularized tumors. They represent the second malignant primary bone tumor of adults after osteosarcoma, but in contrast to osteosarcoma they are resistant to chemotherapy and radiotherapy, surgical excision remaining the only therapeutic option. Few cell lines and animal models are available, and the mechanisms behind their chemoresistance remain largely unknown. Our goal was to establish new cell lines and animal cancer models from human chondrosarcoma biopsies to study their chemoresistance. Between 2007 and 2012, 10 chondrosarcoma biopsies were collected and used for cell culture and transplantation into nude mice. Only one transplanted biopsy and one injected cell line has engrafted successfully leading to conventional central high-grade chondrosarcoma similar to the original biopsies. In culture, two new stable cell lines were obtained, one from a dedifferentiated and one from a grade III conventional central chondrosarcoma biopsy. Their genetic characterization revealed triploid karyotypes, mutations in IDH1, IDH2, and TP53, deletion in CDKN2A and/or MDM2 amplification. These cell lines expressed mesenchymal membrane markers (CD44, 73, 90, 105) and were able to produce a hyaline cartilaginous matrix when cultured in chondrogenic three-dimensional (3D) pellets. Using a high-throughput quantitative RT-PCR approach, we observed that cell lines cultured in monolayer had lost expression of several genes implicated in cartilage development (COL2A1, COMP, ACAN) but restored their expression in 3D cultures. Chondrosarcoma cells in monolayer were sensitive to several conventional chemotherapeutic agents but became resistant to low doses of mafosfamide or doxorubicin when cultured in 3D pellets, in parallel with an altered nucleic accumulation of the drug. Our results indicate that the cartilaginous matrix produced by chondrosarcoma cells may impair diffusion of several drugs and thus contribute to chemoresistance. Therefore, 3D chondrogenic cell pellets constitute a more relevant model to study chondrosarcoma chemoresistance and may be a valuable alternative to animal experimentations.

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Oncostatin M Is a Growth Factor for Ewing Sarcoma

Cited by 37 publications

References 54 publications

IL-38 overexpression induces anti-inflammatory effects in mice arthritis models and in human macrophages in vitro

IL-38 overexpression induces anti-inflammatory effects in mice arthritis models and in human macrophages in vitro

Effect of human papillomavirus 16 oncoproteins on oncostatin M upregulation in oral squamous cell carcinoma

New chondrosarcoma cell lines and mouse models to study the link between chondrogenesis and chemoresistance

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