Role of osteopontin in osteosarcoma

Li, Yusheng; Deng, Zhenhan; Zeng, Chao; Lei, Guanghua

doi:10.1007/s12032-014-0449-y

Cited by 14 publications

(9 citation statements)

References 46 publications

(69 reference statements)

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“…OPN (Osteopontin), also known as SPP1, is a member of the small integrin-binding ligand N-linked glycoprotein (SIBLING) family and is secreted in mammalian cells. Secreted OPN has been discovered in tissue matrix, including bone, fibroblast, osteocyte, dendritic cells, macrophages, and activated T cells [ 22 ]. This study found immunohistochemical expression of OPN protein to be weakly positive in the stromal cells.…”

Section: Discussionmentioning

confidence: 99%

Osteopontin Involves Cisplatin Resistance and Poor Prognosis in Oral Squamous Cell Carcinoma

Luo

Chen

Liu

et al. 2015

BioMed Research International

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Background. Osteopontin (OPN) is a multifunctional cytokine involved in cell survival, migration, and adhesion. However, its role in chemosensitivity in locally advanced oral squamous cell carcinoma (OSCC) in humans has not yet been investigated. Methods. We enrolled 121 patients with locally advanced stage IVA/B OSCC receiving cisplatin-based IC followed by CCRT from January 1, 2006, through January 1, 2012. Immunohistochemistry was used to assess OPN expression in OSCC patients' biopsy specimens from paraffin blocks before treatment. In addition, MTT/colony formation assay was used to estimate the influence of OPN in an oral cancer cell line treated with cisplatin. Results. Of the 121 patients, 94 had positive OPN findings and 52 responded to IC followed by CCRT. Positive osteopontin immunostaining also correlated significantly with positive N status/TNM stage/male gender and smoking. Univariate analyses showed that patients whose tumors had a low expression of OPN were more likely to respond to chemotherapy and have a significantly better OS than those whose tumors had a high expression of OPN. Multivariate analysis revealed that prolonged survival was independently predicted for patients with stage IVA disease, negative lymph nodes, and negative expressions of OPN and for those who received chemotherapy with Docetaxel/cisplatin/fluorouracil (TPF). An oral cancer line stimulated with OPN exhibited a dose-dependent resistance to cisplatin treatment. Conversely, endogenous OPN depletion by OPN-mediated shRNA increased sensitivity to cisplatin. Conclusions. A positive expression of OPN predicts a poor response and survival in patients with locally advanced stage IVA/B OSCC treated with cisplatin-based IC followed by CCRT.

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Section: Discussionmentioning

confidence: 99%

Osteopontin Involves Cisplatin Resistance and Poor Prognosis in Oral Squamous Cell Carcinoma

Luo

Chen

Liu

et al. 2015

BioMed Research International

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“…Furthermore, it is widely held that the earlier these defects occur in the osteoblastic lineage, the more undifferentiated or aggressive the cancer cells [15,19-2 0] . Accordingly, more invasive OS cells are noted to have minimal expression of osteocalcin (OCN) and osteopontin (OPN), both of which are observed at higher levels in mature osteoblasts [21][22][23] . Another notable difference between late osteoprogenitors and OS tumor cells is the ability of the latter to evade senescence through an alternative lengthening of telomere (ALT) pathway [24] .…”

Section: Molecular Basis Of Os and Potential Targets For Therapymentioning

confidence: 99%

Molecular pathogenesis and therapeutic strategies of human osteosarcoma

et al. 2016

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Osteosarcoma (OS) is a devastating illness with rapid rates of dissemination and a poor overall prognosis, despite aggressive standard-of-care surgical techniques and combination chemotherapy regimens. Identifying the molecular mechanisms involved in disease pathogenesis and progression may offer insight into new therapeutic targets. Defects in mesenchymal stem cell differentiation, abnormal expression of oncogenes and tumor suppressors, and dysregulation within various important signaling pathways have all been implicated in development of various disease phenotypes. As such, a variety of basic science and translational studies have shown promise in identifying novel markers and modulators of these disease-specific aberrancies. Born out of these and similar investigations, a variety of emerging therapies are now undergoing various phases of OS clinical testing. They broadly include angiogenesis inhibitors, drugs that act on the bone microenvironment, receptor tyrosine kinase inhibitors, immune system modulators, and other radio- or chemo-sensitizing agents. As new forms of drug delivery are being developed simultaneously, the possibility of targeting tumors locallywhile minimizing systemic toxicityis is seemingly more achievable now than ever. In this review, we not only summarize our current understanding of OS disease processes, but also shed light on the multitude of potential therapeutic strategies the scientific community can use to make long-term improvements in patient prognosis.

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“…Furthermore, it is widely held that the earlier these defects occur in the osteoblastic lineage, the more undifferentiated or aggressive the cancer cells [ 15 , 19 - 20 ] . Accordingly, more invasive OS cells are noted to have minimal expression of osteocalcin (OCN) and osteopontin (OPN), both of which are observed at higher levels in mature osteoblasts [ 21 - 23 ] . Another notable difference between late osteoprogenitors and OS tumor cells is the ability of the latter to evade senescence through an alternative lengthening of telomere (ALT) pathway [ 24 ] .…”

Section: Molecular Basis Of Os and Potential Targets For Therapymentioning

confidence: 99%

Molecular pathogenesis and therapeutic strategies of human osteosarcoma

Sahitya¹,

Denduluri²,

Zhongliang³

et al. 2016

J Biomed Res

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Osteosarcoma (OS) is a devastating illness with rapid rates of dissemination and a poor overall prognosis, despite aggressive standard-of-care surgical techniques and combination chemotherapy regimens. Identifying the molecular mechanisms involved in disease pathogenesis and progression may offer insight into new therapeutic targets. Defects in mesenchymal stem cell differentiation, abnormal expression of oncogenes and tumor suppressors, and dysregulation within various important signaling pathways have all been implicated in development of various disease phenotypes. As such, a variety of basic science and translational studies have shown promise in identifying novel markers and modulators of these disease-specific aberrancies. Born out of these and similar investigations, a variety of emerging therapies are now undergoing various phases of OS clinical testing. They broadly include angiogenesis inhibitors, drugs that act on the bone microenvironment, receptor tyrosine kinase inhibitors, immune system modulators, and other radio- or chemo-sensitizing agents. As new forms of drug delivery are being developed simultaneously, the possibility of targeting tumors locally while minimizing systemic toxicityis is seemingly more achievable now than ever. In this review, we not only summarize our current understanding of OS disease processes, but also shed light on the multitude of potential therapeutic strategies the scientific community can use to make long-term improvements in patient prognosis.

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Role of osteopontin in osteosarcoma

Cited by 14 publications

References 46 publications

Osteopontin Involves Cisplatin Resistance and Poor Prognosis in Oral Squamous Cell Carcinoma

Osteopontin Involves Cisplatin Resistance and Poor Prognosis in Oral Squamous Cell Carcinoma

Molecular pathogenesis and therapeutic strategies of human osteosarcoma

Molecular pathogenesis and therapeutic strategies of human osteosarcoma

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