Sandbox Reserved 830: Difference between revisions
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Defects in OSM and OSMR impact metastatic melanoma cell lines due to the PKC Δ-dependent phosphorylation of Ser727 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<ref name="two"> PMID: 24381786 </ref>. | Defects in OSM and OSMR impact metastatic melanoma cell lines due to the PKC Δ-dependent phosphorylation of Ser727 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<ref name="two"> PMID: 24381786 </ref>. | ||
Defects in OSM 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 | Defects in OSM 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 STAT-3. <ref name="four"> PMID: 12218157 </ref> | ||
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. | 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. | ||