Erik Sahai

Tumour Cell Biology Laboratory

The focus of our research is on the spread of cancer through the body and how the tumour microenvironment affects this process. More recently, we have also become interested in how the tumour microenvironment might be modulated by chemotherapy and how it can affect responses to therapy. Because all of these processes happen within an organism, getting mechanistic data about the molecular basis of processes involved, as opposed to simply measuring the end-point of tumour growth, presents a formidable challenge.

Our group combines genetic and molecular analysis of cell motility and signalling with state-of-the-art imaging technologies - particularly intravital microscopy - to visualise moving cells and when and where signal pathways are active in tumours. These approaches allow us to test the mechanistic predictions generated in our reductionist cell and tissue culture experiments. We are also starting to underpin this work with theoretical models that allow for the exploration new hypotheses and, ultimately, the development of predictive models of cancer cell behaviour.

Figure 1

Two breast cancer cells transfected with the phosphatase regulatory subunit PPP1R14C (in blue) and stained for F-actin (in red) 80x80microns (adapted from Madsen et al Nature Cell Biology 2014). (Click to view larger image)

Selected publications

Madsen CD, Hooper S , Tozluoglu M , Bates PA, Georgina Fletcher G, Barry Thompson B, and Sahai E. STRIPAK components determine mode of cancer cell migration and metastasis. Nature Cell Biology. 2015 Jan;17(1):68-80.

Calvo F, Ege N, Grande-Garcia A, Hooper S, Jenkins RP, Chaudhry SI, Harrington K, Williamson P, Moeendarbary E, Charras G, Sahai E. Mechanotransduction and YAP-dependent matrix remodelling is required for the generation and maintenance of cancer-associated fibroblasts. Nature Cell Biology. 2013;15(6):637-46

Tozluoğlu M, Tournier AL, Jenkins RP, Hooper S, Bates PA, Sahai E. Matrix geometry determines optimal cancer migration strategy and modulates response to interventions. Nature Cell Biology. 2013;15(7):751-62

Hidalgo-Carcedo C, Hooper S, Chaudhry SI, Williamson P, Harrington K, Leitinger B, Sahai E. Collective cell migration requires suppression of actomyosin at cell-cell contacts mediated by DDR1 and the cell polarity regulators Par3 and Par6. Nat Cell Biol. 2011;13(1):49-58

Giampieri S, Jones L, Hill CS, Sahai E. Localised and reversible TGFbeta signalling during metastasis promotes the switch from cohesive to single cancer cell motility. Nat Cell Biol. 2009;11(11):1287-96

Gaggioli C, Hooper S, Hidalgo-Carcedo C, Grosse R, Marshall JF, Harrington K, Sahai E. Fibroblast-led collective invasion of carcinoma cells with differing roles for RhoGTPases in leading and following cells. Nature Cell Biology. 2007;9(12):1392-400

Erik Sahai
+44 (0)20 379 61322

  • Qualifications and history
  • 1998 PhD in Biochemistry, University College, London, UK
  • 1998 Postdoctoral Fellow, Institute of Cancer Research, UK
  • 2003 Postdoctoral Fellow, Albert Einstein College of Medicine, USA
  • 2004 Established lab at the London Research Institute, Cancer Research UK
  • 2015 Group Leader, the Francis Crick Institute, London, UK