Jong-Ho Lee
서울대학교 의과대학 · 의학
이 교수의 연구실은 종양 미세환경과 대사 재편을 중심으로 암의 발병 기전을 규명하고 있으며, 특히 글리코실화 대사 조절 단백질인 PFK1의 이소형이 뇌신생물에서 어떻게 기능하는지 연구하고 있습니다. 또한 나노소재 기반의 생체재료, 특히 감소형 그래핀 산화물과 하이드로우라파이트 복합체를 활용해 골세포 유도 및 뼈 재생을 유도하는 새로운 생체재료 전략을 개발하고 있습니다. 이와 더불어 종양의 뼈 전이를 조절하는 화학유인단백질(CXCL10)의 기능을 규명하여, 암 전이의 분자 기전을 밝혀내는 데에도 기여하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Phosphofructokinase 1 (PFK1) plays a critical role in glycolysis; however, its role and regulation in tumorigenesis are not well understood. Here, we demonstrate that PFK1 platelet isoform (PFKP) is the predominant PFK1 isoform in human glioblastoma cells and its expression correlates with total PFK activity. We show that PFKP is overexpressed in human glioblastoma specimens due to an increased stability, which is induced by AKT activation resulting from phosphatase and tensin homologue (PTEN) l
Recently, graphene-based nanomaterials, in the form of two dimensional substrates or three dimensional foams, have attracted considerable attention as bioactive scaffolds to promote the differentiation of various stem cells towards specific lineages. On the other hand, the potential advantages of using graphene-based hybrid composites directly as factors inducing cellular differentiation as well as tissue regeneration are unclear. This study examined whether nanocomposites of reduced graphene ox
Reduced graphene oxide-coated hydroxyapatite (rGO-coated HAp) composites stimulated the spontaneous osteogenesis in human mesenchymal stem cells in the absence of osteoinductive agents.
Amplification of the chemokines CXCL10 and RANKL has been suggested to promote osteoclast differentiation and osteolytic bone metastasis, but a function for endogenous CXCL10 in these processes is not well established. In this study, we show that endogenous CXCL10 is critical to recruit cancer cells to bone, support osteoclast differentiation and promote for the formation of osteolytic bone metastases. Neutralizing CXCL10 antibody reduced migration of cancer cells expressing the CXCL10 receptor
