Yonsei University · Medicine
Jae-Ho Cheong 교수의 연구실은 종양의 대사 재편성과 에너지 대사에 초점을 맞춰, 암세포의 생존과 치료 저항성 메커니즘을 규명하고 있습니다. 특히 글리콜리시스와 산화적 인산화 과정에서의 에너지 대사 변화, 라이드 옥시드화 스트레스 조절 메커니즘을 통해 암세포자궁세포(CSCs)의 내성 원리를 밝혀내고 있습니다. 이를 기반으로 약물 저항성 극복을 위한 표적 치료 전략 개발을 지속적으로 진행하고 있습니다.
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Tumor cell proliferation requires both growth signals and sufficient cellular bioenergetics. The AMP-activated protein kinase (AMPK) pathway seems dominant over the oncogenic signaling pathway suppressing cell proliferation. This study investigated the preclinical efficacy of targeting the tumor bioenergetic pathway using a glycolysis inhibitor 2-deoxyglucose (2DG) and AMPK agonists, AICAR and metformin. We evaluated the in vitro antitumor activity of 2DG, metformin or AICAR alone, and 2DG in co
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Increased oxidative phosphorylation (OXPHOS) and reactive oxygen species (ROS) levels are inherently linked. ROS are essential signaling molecules, with detrimental effects when produced in excess during chemotherapy, leading to cell death. Cancer stem-like cells (CSCs) are a subpopulation of tumor cells resistant to chemotherapy, highly invasive and metastagenic, driving malignant cancer behavior. In this study, we demonstrated that CSCs exhibit increased OXPHOS but paradoxically low ROS levels
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