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发布于:2018-2-10 01:09:16  访问:1 次 回复:0 篇
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A Number Of Bortezomib Recommendations It Is Advisable To Keep In Mind
Inhibition of gamma-secretase reversed osteoclastogenic effects of breast cancer derived factors and prevented breast cancer cell attachment to osteoblasts, but could not fully rescue breast cancer-induced inhibition of osteoblast differentiation. To explore alternative targets of gamma-secretase activity, we assessed the involvement of amyloid precursor proteins (APP), which were recently shown to play a role in osteoblast attachment. We have found that exposure of osteoblastic cultures to breast cancer factors resulted in decrease in the high molecular weight APP, as assessed by immunoblotting, which corresponded with an increase in immunofluorescence intensity of APP selleck screening library labelling in non-permeabilized cultures. These cancer-induced changes in APP amount and localization were reversed by the inhibition of gamma-secretase. These data suggest that cleavage of APP may play a role in a breast cancer factors-induced breast cancer cell attachment to immature osteoblasts. Thus, our data uncovered osteoblasts as critical intermediary of pre-metastatic signaling by breast cancer cells and BLU 9931 suggest that gamma-secretase is a robust target for developing therapeutics potentially capable of reducing both homing and progression of cancer metastases to bone. Disclosures: Jenna Fong, None. SU0133 Vitamin D Deficiency Promotes Human Prostate Cancer Growth in a Murine Model of Bone Metastasis.Yu Zheng*1, Hong Zhou2, Li Ooi3, Daniel Snir4, Colin Dunstan3, Markus Seibel2. 1Bone Research Program, ANZAC Research Institute, University of Sydney, Australia, 2Bone Research Program, ANZAC Research Institute, The University of Sydney, Australia, 3University of Sydney, Australia, 4University od Sydney, Australia Prostate cancer has a high propensity to metastasise to the skeleton where the bone microenvironment plays a pivotal role in supporting metastatic cancer cell growth. Vitamin D (vitD) deficiency has recently been shown to enhance breast cancer growth in an osteolytic model of breast cancer bone metastasis 1. In the current in vivo study, we investigated the effect vitD-deficiency on prostate cancer cell growth in bone. Three-week old male nude mice were either weaned onto a vitD-free Bortezomib datasheet diet or kept on normal chow. Animals on a vitD-free diet developed hypovitaminosis D within 6 weeks (mean serum 25OH-vitD level 6.9 �� 1.8nmol/L vs. 97.9 �� 10nmol/L in controls; p< 0.01). At steady state, 50000 cells of the prostate cancer cell line PC-3 were injected intra-tibially into vitD-deficient and vitD-replete mice (n=9). Animals were monitored for lytic/sclerotic skeletal lesions by x-ray on days 21, 28 & 35, and tibiae were analysed by micro-CT and histological analyses at endpoint (day 35). Osteoprotegerin (OPG) was co-administered at a dose of 3mg/kg every 3 days in a subset of mice (n=9) to determine the contribution of the bone microenvironment to tumor growth.
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