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Understanding c-Met endosomal signalling in cancer

Dates:31 October 2017
Times:13:00 - 14:00
What is it:Seminar
Organiser:Faculty of Biology, Medicine and Health
Who is it for:University staff, Current University students
Speaker:Stéphanie Kermorgant
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  • In category "Seminar"
  • By Faculty of Biology, Medicine and Health

RTKs contribute to many facets of cell behaviour which play integral roles in tumour development and progression. It is increasingly recognized that RTKs continue their signalling life cycle post-endocytosis, while trafficking through endosomal compartments. The RTK c-Met, (hepatocyte growth factor (HGF) receptor), is overexpressed in many cancers including breast (20-30%) and pancreatic (60-80%) cancers, with levels of expression correlating with poor prognosis. Importantly, c-Met contributes to resistance to existing therapies such as gemcitabine in pancreatic cancer. We demonstrated that the signalling on endosomes of c-Met plays a central role in cell migration, growth and malignant transformation (Kermorgant and Parker, J Cell Biol 2008, Joffre et al., Nat Cell Biol, 2011, Menard et al., Nat Commun, 2014). More surprisingly, we discovered that, in several cell systems, c-Met and beta1-integrin co-internalise and accumulate on endomembranes positive for LC3B (Microtubule-associated protein 1A/1B-light chain 3) and Beclin1, autophagy markers. Our current model is that from these autophagic molecules, c-Met sustains signalling leading to increase survival in anoikis (Barrow-McGee et al. Nat Commun, 2016). Currently, we are analyzing c-Met endosomal signalling in breast and pancreatic cancer. Our work may lead to the development of strategies to reduce the signalling of c-Met in cancer.

Speaker

Stéphanie Kermorgant

Organisation: Barts Cancer Institute

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Michael Smith Lecture Theatre
Michael Smith Building
Manchester

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Anna Fildes

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anna.fildes@manchester.ac.uk

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