Do‐Hyun Nam
성균관대학교 의료기기산업학과 · 의학
남도현 교수의 연구실은 뇌신경종양, 특히 고급도 뇌신생물인 간질성 뇌종양(Glioblastoma, GBM)의 악성화 기전과 치료 저항성 메커니즘을 중심으로 연구를 진행하고 있습니다. c-Met 수용체, Wnt/β-catenin 경로, TGM2 및 Notch 신호전달 경로 등 암세포의 간질성 전환, 생존 및 전이를 조절하는 핵심 분자 기전을 규명하고 있으며, 특히 난이도 높은 종양 미세환경(예: 괴사성 환경)이 암세포의 악성도를 어떻게 조절하는지에 초점을 맞추고 있습니다. 이는 새로운 표적 치료 전략 개발에 기여할 임상의미 있는 통찰을 제공합니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
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.
