Sungkyunkwan University · Medicine
Professor Do-Hyun Nam's research lab focuses on the molecular mechanisms underlying glioblastoma (GBM) pathogenesis, with a particular emphasis on tumor microenvironment interactions, glioma stem cell plasticity, and signaling pathways driving malignancy and therapy resistance. The lab investigates key regulators such as c-Met, Wnt/β-catenin, TGM2, and Notch signaling in promoting tumor invasiveness, mesenchymal transition, and brain metastasis. Their work integrates molecular oncology with translational insights to identify novel therapeutic targets for aggressive brain tumors.
Figures are computed from collected data and may differ slightly.
The authors suggest that c-Met overexpression is associated with shorter survival time and poor treatment response in glioblastomas, the mechanism for which is elevated tumor invasiveness on the molecular and clinical phenotypes. This implies that more effective therapeutic strategies targeting c-Met receptors may have important clinical implication.
These data suggest that Wnt/β-catenin signaling is a key downstream effector of MET signaling and contributes to the maintenance of GSC and GBM malignancy.
Necrosis is a hallmark of glioblastoma (GBM) and is responsible for poor prognosis and resistance to conventional therapies. However, the molecular mechanisms underlying necrotic microenvironment-induced malignancy of GBM have not been elucidated. Here, we report that transglutaminase 2 (TGM2) is upregulated in the perinecrotic region of GBM and triggered mesenchymal (MES) transdifferentiation of glioma stem cells (GSC) by regulating master transcription factors (TF), such as C/EBPβ, TAZ, and ST
Taken together, these results suggest that we have isolated variants of a human cancer cell line with enhanced brain metastatic properties, and the activation of Notch signaling might play a crucial role in brain metastasis.
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