Fibroblast growth factor 2 regulates bone sialoprotein gene transcription in human breast cancer cells

Li, Zhengyang; Wang, Zhitao; Yang, Li; Li, Xinyue; Sasaki, Yohei; Wang, Shuang; Araki, Shouta; Mezawa, Masaru; Takai, Hideki; Nakayama, Youhei; Ogata, Yorimasa

doi:10.2334/josnusd.52.125

Cited by 9 publications

(8 citation statements)

References 40 publications

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“…BSP production in malignant cells may be stimulated by fibroblast growth factor 2 (FGF2). For example, treatment of the human breast cancer cell line MCF7 with FGF2 in vitro results in increased IBSP transcription through activation of CRE2 and AP1 elements in the IBSP promoter [28]. Similar studies demonstrate FGF2 and forskolin (an activator of adenylate cyclase) stimulate in vitro IBSP transcription and BSP protein expression in DU145 human prostate cancer cells [29].…”

Section: Bone Sialoproteinmentioning

confidence: 96%

Bone sialoprotein and osteopontin in bone metastasis of osteotropic cancers

Krüger

Miller

Godwin

et al. 2014

Critical Reviews in Oncology/Hematology

104

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The mechanisms underlying malignant cell metastasis to secondary sites such as bone are complex and no doubt multifactorial. Members of the small integrin-binding ligand N-linked glycoproteins (SIBLINGs) family, particularly bone sialoprotein (BSP) and osteopontin (OPN), exhibit multiple activities known to promote malignant cell proliferation, detachment, invasion, and metastasis of several osteotropic cancers. The expression level of BSP and OPN is elevated in a variety of human cancers, particularly those that metastasize preferentially to the skeleton. Recent studies suggest that the “osteomimicry” of malignant cells is not only conferred by transmembrane receptors bound by BSP and OPN, but includes the “switch” in gene expression repertoire typically expressed in cells of skeletal lineage. Understanding the role of BSP and OPN in tumor progression, altered pathophysiology of bone microenvironment, and tumor metastasis to bone will likely result in development of better diagnostic approaches and therapeutic regimens for osteotropic malignant diseases.

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Section: Bone Sialoproteinmentioning

confidence: 96%

Bone sialoprotein and osteopontin in bone metastasis of osteotropic cancers

Krüger

Miller

Godwin

et al. 2014

Critical Reviews in Oncology/Hematology

104

View full text Add to dashboard Cite

show abstract

“…Both Fra-1 and c-Jun, as AP-1 transcription factor components, have been shown to positively regulate osteoblastic genes, including MGP, BSP, MMP-13 and OCN. 1,12,22,28 Expression of Fos and Jun mRNA and proteins have been reported throughout in vitro osteoblast proliferation and differentiation. 32,33 In vivo , c-Jun transgenic mice showed no bone pathology, 18 but somatic inactivation of c-Jun was found to result in mice with malformed axial skeletons, 6 while transgenic expression or conditional knockout of Fra-1 results in mice with increased or decreased bone formation rates respectively.…”

Section: Discussionmentioning

confidence: 99%

Enhancement of Flow-Induced AP-1 Gene Expression by Cyclosporin A Requires NFAT-Independent Signaling in Bone Cells

et al. 2014

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Growing evidence suggests that aging compromises the ability of the skeleton to respond to anabolic mechanical stimuli. Recently, we reported that treating senescent mice with Cyclosporin A (CsA) rescued aging-related deficits in loading-induced bone formation. Given that the actions of CsA are often attributed to inhibition of the calcineurin/NFAT axis, we hypothesized that CsA enhances gene expression in bone cells exposed to fluid flow, by inhibiting nuclear NFATc1 accumulation. When exposed to flow, MC3T3-E1 osteoblastic cells exhibited rapid nuclear accumulation of NFATc1 that was abolished by CsA treatment. Under differentiation conditions, intermittent CsA treatment enhanced gene expression of late osteoblastic differentiation markers and activator protein 1 (AP-1) family members. Superimposing flow upon CsA further enhanced expression of the AP-1 members Fra-1 and c-Jun. To delineate the contribution of NFAT in this response, cells were treated with VIVIT, a specific inhibitor of the calcineurin/NFAT interaction. Treatment with VIVIT blocked flow-induced nuclear NFATc1 accumulation but did not recapitulate the CsA-mediated enhancement of flow-induced AP-1 component gene expression. Taken together, our study is the first to demonstrate that CsA enhances mechanically-induced gene expression of AP-1 components in bone cells, and suggests that this response requires calcineurin-dependent mechanisms that are independent of inhibiting NFATc1 nuclear accumulation.

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“…[20,21] Many factors, including hormones, growth factors and cytokines, may interfere in regulating BSP transcription through tyrosine kinase, mitogenactivated protein kinase and cAMP-dependent pathways. [22][23] Obtained data indicate BSP as an intriguing, multifunctional protein mainly involved in bone metabolism. In summary, BSP may intervene at several steps of bone remodeling by its capability to nucleate hydroxyapatite crystal formation under steady-state conditions, promote mineralization of some osteoblastic cell lines, induce osteoblast and osteoclast adhesion and increase osteoclastogenesis and bone resorption.…”

Section: Bone Sialoprotein: a Multifunctional Proteinmentioning

confidence: 92%

Serum bone sialoprotein levels and bone metastases

et al. 2011

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The skeleton is the most common site of tumor metastasis. The detection of metastatic bone disease is critical for primary cancer staging because it will condition the therapeutic decision and the prognosis. For the diagnosis of bone metastases, imaging techniques are usually employed, even if these techniques have some limitations in terms of accuracy and costs. An innovative, cheaper method for the screening of skeletal metastases could be the measurement of bone turnover markers. This article is aimed at providing a literature review on the clinical significance of increased serum levels of bone sialoprotein (BSP) observed in patients suffering from metastatic bone lesions. In addition, we have briefly summarized recent studies reporting the biological and pathological roles of BSP in bone remodeling and bone metastasis. Some studies have demonstrated that serum BSP can be considered as an early marker and a prognostic factor for the development of bone metastases. BSP may help in assessing osteolytic bone disease, in evaluating additional prognostic information and in monitoring treatment modalities.

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Fibroblast growth factor 2 regulates bone sialoprotein gene transcription in human breast cancer cells

Cited by 9 publications

References 40 publications

Bone sialoprotein and osteopontin in bone metastasis of osteotropic cancers

Bone sialoprotein and osteopontin in bone metastasis of osteotropic cancers

Enhancement of Flow-Induced AP-1 Gene Expression by Cyclosporin A Requires NFAT-Independent Signaling in Bone Cells

Serum bone sialoprotein levels and bone metastases

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