Current projects
Mitochondrial Fusion Controls Cancer Cell Survival
Mitochondria constantly remodel their structure through opposing processes known as fission and fusion. This dynamic behavior is essential for maintaining a healthy population of mitochondria and sustaining cellular metabolism. In cancer cells, however, mitochondrial dynamics can be co-opted to support growth, metabolic flexibility, and resistance to stress. Our research focuses on how mitochondrial fusion, controlled by the inner-membrane protein OPA1, shapes cellular metabolism and survival. We have found that disrupting OPA1 strongly suppresses the growth of breast cancer cells, revealing an unexpected link between mitochondrial architecture and metabolic fitness. These findings suggest that mitochondrial fusion may represent an important vulnerability in cancer. Our goal is to understand how mitochondrial structure controls metabolic signaling and to explore whether targeting mitochondrial fusion can limit tumor growth or enhance the effectiveness of chemotherapy.
protein interaction mapping
pathways of similar co-dependencies from cancer cell CRISPR screens
Cancer cells differ dramatically in how they rely on mitochondrial function. While some tumors are remarkably dependent on mitochondrial fusion to maintain metabolism and survival, others appear able to compensate when this pathway is disrupted. This raises a fundamental question: what cellular programs allow cancer cells to tolerate or resist loss of mitochondrial fusion?
Our research seeks to uncover the stress-response pathways that are coordinated by mitochondrial fusion and that determine whether a cancer cell survives or collapses when mitochondrial architecture is disrupted. By integrating mechanistic studies with large-scale CRISPR gene-dependency datasets across diverse cancer cell lines, we aim to identify the cellular networks that make certain tumors uniquely dependent on mitochondrial fusion.
Understanding these relationships may reveal new metabolic vulnerabilities in cancer and suggest strategies to exploit mitochondrial stress pathways to suppress tumor growth or enhance the effectiveness of existing therapies.
Our current research aims to address:
How does mitochondrial fusion support the metabolic resilience of cancer cells?
What stress-response pathways become activated when mitochondrial architecture is disrupted?
Can these mitochondrial stress mechanisms be exploited to selectively eliminate cancer cells?