Sandbox Reserved 830: Difference between revisions
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OSM is a compact molecule with dimensions of approximately 20 Å x 27 Å x 56 Å, that fit with the up-up-down-down four-helix bundle structure. | OSM is a compact molecule with dimensions of approximately 20 Å x 27 Å x 56 Å, that fit with the up-up-down-down four-helix bundle structure. | ||
[[Image:Oncostatin structure.png|frame| | [[Image:Oncostatin structure.png|frame|left|Ribbon colored diagram of hOSM from N-terminus in blue to the C-terminus in red. The two disulphide bonds are shown as ball-and-sticks models with the sulphur atoms represented as yellow spheres. The CD loop as observed in LIF is represented by the transparent dotted section.]] [[Image:Oncostatin structure2.png|frame|center|Stereodiagram of the Cα trace for hOSM.]] | ||
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==Disease== | ==Disease== | ||
Oncostatin M is a pleiotropic protein and it takes part in the regulation of several organ systems. Thus, OSM is involved in a lot of pathologies mainly due to its large signaling functions targeting so many different cell types. OSM impacts cell proliferation and stimulate angiogenesis, thus its alterations greatly increase the risks of tumor growth and cancer development. | Oncostatin M is a pleiotropic protein and it takes part in the regulation of several organ systems. Thus, OSM is involved in a lot of pathologies mainly due to its large signaling functions targeting so many different cell types. OSM impacts cell proliferation and stimulate angiogenesis, thus its alterations greatly increase the risks of tumor growth and cancer development. | ||
Defects in OSM and OSMR impact metastatic melanoma cell lines due to the PKC Δ-dependent phosphorylation of Ser 727 on STAT-3 and other signaling pathways. Moreover some epigenetic mechanisms have been shown to be responsible for altering the nature of metastatic melanoma, increasing OSMR expression and responsiveness of the cells. | Defects in OSM and OSMR impact metastatic melanoma cell lines due to the PKC Δ-dependent phosphorylation of Ser 727 on STAT-3 and other signaling pathways. Moreover some epigenetic mechanisms have been shown to be responsible for altering the nature of metastatic melanoma, increasing OSMR expression and responsiveness of the cells. | ||
Defects in OMS induce high levels of osteoblasts and osteoblast markers in differentiated osteosarcoma cells dramatically enhancing the proliferation of osteosarcoma cells, while stimulating an invasive phenotypic alteration of these cells mainly by the MMP-2 and VEGF expression, mediated by STAT3. | Defects in OMS induce high levels of osteoblasts and osteoblast markers in differentiated osteosarcoma cells dramatically enhancing the proliferation of osteosarcoma cells, while stimulating an invasive phenotypic alteration of these cells mainly by the MMP-2 and VEGF expression, mediated by STAT3. | ||
OSM has been shown to stimulate the proliferation of Ewing sarcoma cell lines, 22Rv1 prostate cancer cells, SKOV3 ovarian cancer cells, while an increase in OSMR expression has been found in cervical carcinoma. OSMR modifications were found to enhance human lung carcinoma development by reducing the cells’ sensitivity to OSM. Epigenetic mutations, such as methylation, cause the silencing of OSMR, thus the inhibition of both colon cancer cell lines and papillary thyroid cancer cell proliferation. | |||
OSM has been shown to stimulate the proliferation of Ewing sarcoma cell lines, 22Rv1 prostate cancer cells, SKOV3 ovarian cancer cells, while an increase in OSMR expression has been found in cervical carcinoma. | |||
OSMR modifications were found to enhance human lung carcinoma development by reducing the cells’ sensitivity to OSM. | |||
Epigenetic mutations, such as methylation, cause the silencing of OSMR, thus the inhibition of both colon cancer cell lines and papillary thyroid cancer cell proliferation. | |||