Sandbox Reserved 830: Difference between revisions

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Activation of those pathways stimulates several responses. The main one is proliferation of a lot of different cell lines by increasing production of molecules, such as proliferation factors and metalloproteinase inhibitors. In endothelial cells, vascular endothelial growth factors (VEGF) are secreted, promoting angiogenesis. Binding of OSM induces inhibition of other cell proliferation, like stem cells or tumor cells, by blocking the cell cycle in G2/M<ref name="three"> PMID: 10446061 </ref>. Binding of OSM ~~grant~~ an invasive phenotype of cells by stimulation of chemokine secretion (like eotaxin). Chemokine allows activation of immune cells as well, and then stimulates the production of antibodies<ref name="two"> PMID: 24381786 </ref>. Physiological function of OSM in the central nervous system remains unknown<ref group=""> PMID: 14985435 </ref>.

Activation of those pathways stimulates several responses. The main one is proliferation of a lot of different cell lines by increasing production of molecules, such as proliferation factors and metalloproteinase inhibitors. In endothelial cells, vascular endothelial growth factors (VEGF) are secreted, promoting angiogenesis. Binding of OSM induces inhibition of other cell proliferation, like stem cells or tumor cells, by blocking the cell cycle in G2/M<ref name="three"> PMID: 10446061 </ref>. Binding of OSM grants an invasive phenotype to cells by stimulation of chemokine secretion (like eotaxin). Chemokine allows activation of immune cells as well, and then stimulates the production of antibodies<ref name="two"> PMID: 24381786 </ref>. Physiological function of OSM in the central nervous system remains unknown<ref group=""> PMID: 14985435 </ref>.

Line 50:

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<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 ~~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~~. <ref name="four"> PMID: 12218157 </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 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.

Sandbox Reserved 830: Difference between revisions

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@@ Line 44: / Line 44: @@
-Activation of those pathways stimulates several responses. The main one is proliferation of a lot of different cell lines by increasing production of molecules, such as proliferation factors and metalloproteinase inhibitors.  In endothelial cells, vascular endothelial growth factors (VEGF) are secreted, promoting angiogenesis. Binding of OSM induces inhibition of other cell proliferation, like stem cells or tumor cells, by blocking the cell cycle in G2/M<ref name="three"> PMID: 10446061 </ref>. Binding of OSM grant an invasive phenotype of cells by stimulation of chemokine secretion (like eotaxin). Chemokine allows activation of immune cells as well, and then stimulates the production of antibodies<ref name="two"> PMID: 24381786 </ref>. Physiological function of OSM in the central nervous system remains unknown<ref group=""> PMID: 14985435 </ref>.
+Activation of those pathways stimulates several responses. The main one is proliferation of a lot of different cell lines by increasing production of molecules, such as proliferation factors and metalloproteinase inhibitors.  In endothelial cells, vascular endothelial growth factors (VEGF) are secreted, promoting angiogenesis. Binding of OSM induces inhibition of other cell proliferation, like stem cells or tumor cells, by blocking the cell cycle in G2/M<ref name="three"> PMID: 10446061 </ref>. Binding of OSM grants an invasive phenotype to cells by stimulation of chemokine secretion (like eotaxin). Chemokine allows activation of immune cells as well, and then stimulates the production of antibodies<ref name="two"> PMID: 24381786 </ref>. Physiological function of OSM in the central nervous system remains unknown<ref group=""> PMID: 14985435 </ref>.
@@ Line 50: / Line 50: @@
 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<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 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. <ref name="four"> PMID: 12218157 </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 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.