O akci
Mitochondria are central to cell fate decisions and the regulation of cell death. Defects in apoptosis initiation at the mitochondria can promote tumorigenesis and render cancer cells broadly resistant to various chemotherapeutics. We have recently identified a novel mitochondria-mediated mechanism of cancer multidrug resistance, which involves the loss of mitochondria–endoplasmic reticulum contacts, leading to apoptotic insensitivity. Thus, our current research focuses on exploring selective mitochondrial vulnerabilities that could be therapeutically targeted to directly overcome multidrug resistance at the mitochondrial level for the treatment of refractory childhood tumors. Mitochondria are highly dynamic organelles that constantly undergo various adjustments, including fission, fusion, biogenesis, and mitophagy, which collectively modulate mitochondrial function and maintain healthy mitochondria in both normal and tumor cells. In my talk, I will discuss our recent insights into the therapeutic potential of targeting mitochondrial biogenesis, namely the mitochondrial gene expression machinery, and mitochondrial fission in aggressive childhood tumors. Finally, I will outline the novel concept of mitoribosomal synthetic lethality and introduce our newly established models of tunable MYC protein expression to study MYC-dependent mitochondrial vulnerabilities, while avoiding the limitations of existing systems that rely on inducers known to interfere with mitochondrial functions.
Více informací
This event is part of the Principal Investigator Seminar Series, the schedule of seminars can be found here.
