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Israt Jahan Tulip,김성옥,김은정,김재봉,이재용,김형기,김성찬 한국통합생물학회 2021 Animal cells and systems Vol.25 No.3
Glioblastoma multiforme (GBM) is the most aggressive primary brain cancer and this is due to cancer cells being apoptosis-resistant and having increased cell proliferation, migration, invasion, and angiogenesis properties. Previous studies have indicated both STAT and Notch pathways being important for initiation and progression in GBM. In this work, we first studied the effects of STAT inhibitors on Notch signalling using small molecule STAT inhibitors. It was observed that STAT inhibitors surprisingly activated Notch signalling by inducing NICD and Notch target genes in GBM cells. Thus, we aimed to combine STAT inhibitor treatment with a Notch pathway inhibitor and study effects on GBM tumourigenesis. STAT5 inhibitor (Pimozide) and STAT3 inhibitor (S3I- 201) were individually used in combination with γ-secretase inhibitor (DAPT), an inhibitor of Notch signalling, in a panel of GBM cells for cell proliferation and epithelial plasticity changes. Compared with single-agent treatments, combinatorial treatments with the STAT and Notch inhibitors significantly increased apoptosis in the treated cells, impairing cell proliferation, migration, and invasion. These findings suggest that concurrent blocking of STAT and Notch signalling pathways could provide added therapeutic benefit for the treatment of glioblastoma.
The role for GALNT14 in lung metastasis of breast cancer
Ki-Hoon Song,Mi So Park,Tulip S. Nandu,Shrikanth Gadad,Sang-Cheol Kim,Mi-Young Kim 한국당과학회 2018 한국당과학회 학술대회 Vol.2018 No.01
Polypeptide N-acetyl-galactosaminyltransferases (GALNTs) have been shown to play diverse roles in several biological processes, but their function in organ-tropic metastasis remains unknown. Here, we find that GALNT14expression is specifically associated with pulmonary metastasis in breast cancer patients. Furthermore, we demonstrate that GALNT14 promotes lung metastasis by facilitating two important steps during the metastatic process, i.e., initiation of metastatic colonies and their subsequent growth into overt metastases. Mechanistic studies suggest that GALNT14 not only augments self-renewal of breast cancer cells within the lung microenvironment but also allows breast cancer cells to exploit macrophage-derived growth factors for their continuous growth. The mediators of GALNT14 involved in these processes will also be discussed.