Understanding the mechanisms of ovarian cancer metastasis
Our research examines how ovarian cancer cells acquire metastatic behaviour and establish new tumours. We investigate cell adhesion and plasticity, metabolic interactions with surrounding tissues, and cooperation between distinct tumour cell populations to identify mechanisms that may be therapeutically targeted.
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Cell adhesion molecules influence how cancer cells change state and move. We identified DNM1-dependent recycling of N-cadherin as a mechanism supporting mesenchymal behaviour and metastatic colonisation. This work shows how the handling of adhesion molecules can shape ovarian cancer cell plasticity.
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We study how ovarian cancer cells interact with the mesothelium, which lines the abdominal cavity. Our work showed that P-cadherin-mediated adhesion stimulates lactate production in mesothelial cells. Cancer cells use this lactate for lipid synthesis, linking tissue interactions to metastatic growth.
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Different cancer cell populations can cooperate to promote metastasis. We showed that less metastatic, senescence-like cells release signals that enhance the spread of more metastatic ovarian cancer cells. These findings connect β-catenin/YAP signalling, tumour heterogeneity and potential therapeutic vulnerabilities.
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We combine molecular and cellular experiments with imaging, patient tumour material and preclinical models. By connecting findings across these systems, we aim to understand metastatic mechanisms and identify vulnerabilities for further therapeutic investigation.
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