Therapeutic Strategy Targeting TGF-β-Smad3 Signaling in metastatic can…

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  • 2017-01-06


[2016 Fall Life Sciences & IBB Regular Seminar]
                    ▶Subject: Therapeutic Strategy Targeting TGF-β-Smad3 Signaling in metastatic cancers
                    ▶Speaker: Prof. Seong-Jin Kim (Seoul National University)
                    ▶Date: 4:30PM/Oct. 28(Fri.)/2016
                    ▶Place: Auditorium(1F), POSTECH Biotech Center
                    Transforming growth factor β (TGF-β) affects growth, survival and differentiation of most cell type. Following ligand-induced hetero-tetramerization of type I and type II serine/threonine kinase receptors, Smad2 and 2 are phosphorylated and then they form complexes with Smad4, which are translocated to the nucleus where they regulate the transcription of certain genes. Smad signaling leads to growth arrest as well as epithelial-to-mesenchymal transition (EMT) of epithelial tumor cells. Smad3 functions as both a positive and negative regulator in carcinogenesis. In response to TGF-β the TGF-β receptor phosphorylates serine residues at the Smad3 C-tail. Cancer cells often contain high levels of MAPK and CDK activities, which can lead to the Smad3 linker region becoming highly phosphorylated at the basal state. In vitro/in vivo study revealed that the mutation of the Smad3 linker phosphorylation sites greatly intensifies the TGF-β-induced EMT with an increased invasive activity, growth arrest and apoptosis together with reduction in the size of putative cancer stem cell subpopulation, suggesting that the linker phosphorylation negatively regulates the canonical TGF-β signaling. . In this talk, I will present our recent studies about role of TGF-β signaling in metastasis and cancer stemness, which provide a basis for future clinical studies.

                ▶Inquiry: Prof. Seung-Woo Lee (T. 279-2355)
                      * This seminar will be given in English.
                  please refrain from taking photos during seminars. *