Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0265264 (HOS)
 1,119 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased activity, membrane association, and secretion of cathepsin B have been shown to correlate positively with invasiveness and the metastatic properties of many tumor entities. Cathepsin B is able to directly facilitate invasion by degrading extracellular matrix components or to indirectly facilitate invasion by activating other matrix-degrading proteases like the urokinase-type plasminogen activator. To investigate the role of cathepsin B in bone tumor invasion, the osteosarcoma cell line MNNG/HOS was stably transfected with an expression vector capable of expressing the antisense cDNA transcript of cathepsin B. Five stably transfected antisense cell clones, the control (vector) cell clones, and the parental cells were characterized. At first, the stable incorporation of the constructs was demonstrated by Southern blot analysis. In ELISA assays, all antisense clones showed a significant reduction at the cathepsin B antigen level (about 70%) as compared with the control cell clones and MNNG/HOS. Similar results were obtained for cathepsin B activity in the antisense-transfected cells. In the antisense cell clones, Northern blot analysis and reverse transcription-PCR revealed a considerable decrease of approximately 50% in the levels of cathepsin B mRNA. Expression of cathepsins L and K (sequence homologies) was not affected. The invasive potential and migration of untransfected and transfected tumor cell clones in vitro were analyzed in Transwell chambers. Antisense-transfected cells showed a markedly lower invasion and motility than did MNNG/HOS and the controls. Adhesion to collagen I and matrigel matrices was not affected. These results demonstrate that cathepsin B is involved in the complex proteolytic processes in invasive osteosarcomas.
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PMID:Inhibitory effects of antisense cathepsin B cDNA transfection on invasion and motility in a human osteosarcoma cell line. 1060 50

Hypoxia, inflammation, and acidity occur after bone fracture. To simplify the fracture model, we tested the effects of acidity in osteoblasts. We tested three osteoblast cell lines, MG63, MC3T3E1, and HOS cells, with MG63 cells showing much higher sensitivity to acidic pH. In physiologically acidic surroundings, pH 7.2, the endoplasmic reticulum stress response was measured through the expression of unfolded protein response proteins. Acidic surroundings time-dependently increased IL-6 secretion. Cathepsin B, a marker of the inflammation and angiogenic processes that occur after bone fracture, also increased. Thus, acidity can cause ER stress, increase IL-6, and increases cathepsin B expression in osteoblasts.
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PMID:Acidic pH environments increase the expression of cathepsin B in osteoblasts: the significance of ER stress in bone physiology. 1924 48