bone neoplasms/protease

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Involvement of protease-activated receptor 2 in nociceptive behavior in a rat model of bone cancer.

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Treatment for bone cancer pain remains a clinical challenge due to a poor understanding of the underlying mechanisms. Protease-activated receptor 2 (PAR2), a receptor for inflammatory proteases, has been implicated in nociceptive signaling under both normal and pathologic pain states. However,

Increased expression of protease-activated receptor 2 and 4 within dorsal root ganglia in a rat model of bone cancer pain.

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In an effort to understand the underlying mechanisms of cancer-induced bone pain, we investigated the presence of two protease-activated receptors, protease-activated receptor 2 (PAR2), and protease-activated receptor 4 (PAR4), in dorsal root ganglia (DRGs) neurons in an animal model of bone cancer

Protease-activated receptor 2 in dorsal root ganglion contributes to peripheral sensitization of bone cancer pain.

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BACKGROUND Treating bone cancer pain continues to be a major clinical challenge, and the underlying mechanisms of bone cancer pain remain elusive. Protease-activated receptor 2 (PAR2) has been reported to be involved in neurogenic inflammation, nociceptive pain and hyperalgesia. Here, we

Quantitative analysis of the impact of short-time high hydrostatic pressure on bone tumor-associated proteases.

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In orthopedic surgery, sterilization of bone used for reconstruction of osteoarticular defects caused by malignant tumors is carried out in various ways. At present, to devitalize tumor-bearing osteochondral segments, extracorporeal irradiation or autoclaving is mainly used, although both methods

Engagement of signaling pathways of protease-activated receptor 2 and μ-opioid receptor in bone cancer pain and morphine tolerance.

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Pain is one of the most common and distressing symptoms suffered by patients with progression of cancer. Using a rat model of bone cancer, recent findings suggest that proteinase-activated receptor 2 (PAR2) signaling pathways contribute to neuropathic pain and blocking PAR2 amplifies antinociceptive

Protease-activated receptor 2 antagonist potentiates analgesic effects of systemic morphine in a rat model of bone cancer pain.

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OBJECTIVE Bone cancer pain affects the quality of life of cancer patients. This study was aimed at investigating the analgesic effects of combined therapies with an antagonist of proteinase-activated receptor (PAR) 2 and morphine on pain-related behaviors in a rat model of bone cancer

Expression of cellular FLICE inhibitory protein, caspase-8, and protease inhibitor-9 in Ewing sarcoma and implications for susceptibility to cytotoxic pathways.

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OBJECTIVE Ewing sarcoma is a common pediatric bone tumor with an unfavorable prognosis for metastatic or recurrent disease. Cellular immunotherapy may provide new treatment options and depends on the cytolytic death receptor and perforin/granzyme pathways. Expression of death receptor pathway

Regulation of insulin-like growth factors and IGF-binding proteins in bone tumours.

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Insulin-like growth factors (IGFs) and IGF-binding proteins (IGFBPs) are important regulators of growth and development in normal bone and bone tumours. IGFs contribute to about 50% of basal bone cell proliferation. Their mitogenic actions is either enhanced or inhibited by specific IGFBPs which are

Proteases and bone remodelling.

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Bone remodelling is regulated by osteogenic cells which act individually through cellular and molecular interaction. These interactions can be established either through a cell-cell contact, involving molecules of the integrin family, or by the release of many polypeptidic factors and/or their

Enhanced expression of cathepsin L in metastatic bone tumors.

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Cathepsin L is a kind of cystein proteases which are known to facilitate the invasion and metastasis of tumor cells by degrading the components of basement membrane and extracellular matrix. This study was undertaken to investigate the expression of cathepsin L by Northern blot analysis with

Fusion of the COL1A1 and USP6 genes in a benign bone tumor.

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Aneurysmal bone cyst (ABC) is a benign intraskeletal cyst that often expands rapidly and shows a strong tendency to recur. Rearrangement of chromosome band 17p13 is a characteristic genetic feature of ABC, with t(16;17)(q22;p13) the most frequent chromosomal aberration. This translocation generates

The mechanism of quercetin in regulating osteoclast activation and the PAR2/TRPV1 signaling pathway in the treatment of bone cancer pain.

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The present paper aimed to investigate the therapeutic effect of quercetin in a rat model of bone cancer pain, and to further explore the molecular mechanism of quercetin in the treatment of bone cancer pain.The activation status of the osteoblasts in each

Ubiquitin‑specific protease 7 promotes osteosarcoma cell metastasis by inducing epithelial‑mesenchymal transition.

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Osteosarcoma (OS) is the most common primary malignant bone tumour among adolescents and young adults; however, its molecular pathogenesis has not been completely elucidated. Ubiquitin‑specific protease 7 (USP7), a member of the deubiquitinating enzyme family, plays a role in the malignancy process

Bone cancer pain: causes, consequences, and therapeutic opportunities.

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Common cancers, including cancers of the breast, lung, and prostate, frequently metastasize to multiple bones where they can cause significant and life-altering pain. Similar to cancer itself, the factors that drive bone cancer pain evolve and change with disease progression. Once cancer cells have

The effect of Neovastat (AE-941) on an experimental metastatic bone tumor model.

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Bone metastases are generally associated with bone destruction which occurs in response to factors secreted by metastatic cells. Some of these factors secreted by the metastatic cells activate osteoclats while others are proteases that degrade bone collagen. To determine if Neovastat (AE-941), a

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