Long term oncostatin M treatment induces an osteocyte-like differentiation on osteosarcoma and calvaria cells

Brounais, Bénédicte; David, Emmanuelle; Chipoy, Céline; Trichet, Valérie; Ferré, Virginie; Charrier, Céline; Duplomb, Laurence; Berreur, Martine; Rédini, Françoise; Heymann, Dominique; Blanchard, Frédéric

doi:10.1016/j.bone.2008.12.021

Cited by 25 publications

(11 citation statements)

References 35 publications

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“…OSM has been shown to induce bone loss and sensitized rat osteosarcoma to apoptosis [30] and induce differentiation of chondrosarcoma and osteosarcoma cells [31, 32]. However, several studies show that OSM may enhance tumour progression and metastasis.…”

Section: Discussionmentioning

confidence: 99%

Global Gene Expression Profiling of Human Osteosarcomas Reveals Metastasis-Associated Chemokine Pattern

Namløs

Kresse

Müller

et al. 2012

Sarcoma

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Global gene expression analysis was performed on a panel of 23 osteosarcoma samples of primary and metastatic origin using the Applied Biosystems Gene Expression Array System. When comparing the primary tumours with the metastases, we found a significantly increased expression of genes involved in immunological processes, for example coding for cytokines and chemokines, in the metastatic samples. In addition, a comparison of the gene expression in primary samples from patients with or without metastases demonstrated that patients who later developed metastases had high expression of the chemokine (C-X-C motif) receptor 4 (CXCR4), similar to the metastatic samples, suggesting that these signal molecules play an important role in promoting metastasis. Increased knowledge of mechanisms and interactions between specified molecular signalling pathways in osteosarcomas could lead to a more rational strategy for development of targeted therapy.

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Section: Discussionmentioning

confidence: 99%

Global Gene Expression Profiling of Human Osteosarcomas Reveals Metastasis-Associated Chemokine Pattern

Namløs

Kresse

Müller

et al. 2012

Sarcoma

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“…In contrast, pro-catabolic stimuli appear to increase SCL expression in bone, for example mechanical unloading (Robling et al, 2006) or exposure of osteoblast-lineage cells to pro-inflammatory cytokines such as TNFa and TWEAK Vincent et al, 2009). Another cytokine, oncostatin M, has also been shown to modulate the expression of SCL, depending on whether the exposure is chronic or acute (Brounais et al, 2009;Walker et al, 2010). The hormone 1a,25-dihydroxyvitamin D 3 (1,25D) is an important regulator of calcium homeostasis and is thought to act both at the intestine and in the bone itself.…”

Section: Introductionmentioning

confidence: 86%

1α,25-dihydroxyvitamin D3 stimulates human SOST gene expression and sclerostin secretion

Wijenayaka

Yang

Prideaux

et al. 2015

Molecular and Cellular Endocrinology

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Sclerostin, the SOST gene product, is a negative regulator of bone formation and a positive regulator of bone resorption. In this study, treatment of human primary osteoblasts, including cells differentiated to an osteocyte-like stage, with 1α,25-dihydroxyvitaminD3 (1,25D) resulted in the dose-dependent increased expression of SOST mRNA. A similar effect was observed in human trabecular bone samples cultured ex vivo, and in osteocyte-like cultures of differentiated SAOS2 cells. Treatment of SAOS2 cells with 1,25D resulted in the production and secretion of sclerostin protein. In silico analysis of the human SOST gene revealed a single putative DR3-type vitamin D response element (VDRE) at position -6216 bp upstream of the transcription start site (TSS). This sequence was confirmed to have strong VDRE activity by luciferase reporter assays and electrophoretic mobility shift analysis (EMSA). Sequence substitution in the VDR/RXR half-sites abolished VDRE reporter activity and binding of nuclear proteins. A 6.3 kb fragment of the human proximal SOST promoter demonstrated responsiveness to 1,25D. The addition of the evolutionary conserved region 5 (ECR5), a known bone specific enhancer region, ahead of the 6.3 kb fragment increased basal promoter activity but did not increase 1,25D responsiveness. Site-specific mutagenesis abolished the responsiveness of the 6.3 kb promoter to 1,25D. We conclude that 1,25D is a direct regulator of human SOST gene and sclerostin protein expression, extending the pathways of control of sclerostin expression. At least some of this responsiveness is mediated by the identified classical VDRE however the nature of the transcriptional regulation by 1,25D warrants further investigation.

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“…Samples were loaded on precast 12% Bolt mini gels (Life technologies, Waltham, Massachusetts USA). Primary antibodies (anti-mIL-38, R&D Systems; anti-hIL-38, R&D Systems) were used to detect proteins of interest as described 20 21…”

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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Long term oncostatin M treatment induces an osteocyte-like differentiation on osteosarcoma and calvaria cells

Cited by 25 publications

References 35 publications

Global Gene Expression Profiling of Human Osteosarcomas Reveals Metastasis-Associated Chemokine Pattern

Global Gene Expression Profiling of Human Osteosarcomas Reveals Metastasis-Associated Chemokine Pattern

1α,25-dihydroxyvitamin D3 stimulates human SOST gene expression and sclerostin secretion

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

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