日米共催ウェビナー2025のアーカイブを公開いたしました！
＜本ウェビナーで学べるポイント＞
・フェロトーシスの最新メカニズム
・抵抗性がん治療への応用戦略
・創薬・診断に向けた新しい研究アプローチ
Dojindo日米共催ウェビナー2025アーカイブ: フェロトーシス研究の最前線
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Mechanisms and Therapeutic Targeting of Ferroptosis
James Olzmann
Doris Howes Calloway
Chair and Professor
UC BerkeleyDr. James Olzmann is the Doris H. Calloway Chair and Professor at the University of California, Berkeley. He holds joint appointments in the Departments of Molecular & Cell Biology and Nutritional Sciences & Toxicology. In this seminar, Dr. Olzmann will highlight recent discoveries from his lab on the mechanisms that govern oxidative lipid damage and ferroptosis, a regulated form of cell death. Using genetic screening approaches, his team has identified critical regulators of cellular responses to lipid peroxidation, such as FSP1, an oxidoreductase that functions parallel to GPX4 to recycle membrane antioxidants and suppress ferroptosis. Recent findings also reveal that FSP1 protects neutral lipids in lipid droplets, and that its inhibition sensitizes cancer cells to ferroptosis. These insights uncover key aspects of lipid biology and oxidative stress resilience, while pointing to new therapeutic opportunities. Targeting ferroptosis resistance mechanisms offers a promising strategy to overcome drug resistance in cancer and related diseases.
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Exploring Novel Cell Death Phenotypes in Cancer
Scott Dixon
Professor of Biology
Stanford UniversityNon-apoptotic cell death mechanisms that can be induced by small molecules are of fundamental mechanistic interest and may be useful to treat certain cancers. We have previously identified small molecules (erastin, RSL3) that induce an iron-dependent, non-apoptotic form of cell death termed ferroptosis. Through chemical genetic screening we have identified roles for several lipid metabolic enzymes in this non-apoptotic cell death mechanism. More recently, we have identified a clinical candidate oncology drug that activates a novel, lipid-dependent mechanism of non-apoptotic cell death that is distinct from ferroptosis. This lethal mechanism requires the lipid metabolic enzyme trans-2,3-enoyl-CoA reductase (TECR). TECR is canonically involved in the synthesis of very long chain fatty acids but seems to promote non-apoptotic cancer cell death in response to tegavivint by synthesizing a saturated long-chain fatty acid, palmitate. I will discuss these findings in the context of our overall search for novel ways to induce cancer cell death for the treatment of cancers.
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