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Espin enhances confined migration by inducing filopodia formation and promotes cancer metastasis

ABSTRACT: Cells send out actin-driven protrusions at the leading edge, in forms of lamellipodia and filopodia. Genes regulating filopodia have been implicated in cancer metastasis - a process intimately associated with cell motility. However, cells depleted of lamellipodia but retained filopodia remain minimal motility on 2D surface, obscuring the role of filopodia in cell motility. In confined cell migration - where cells are spatially restricted, the well-known regulating factors include cell blebbing, nuclear deformation and rear contractility, without much emphasis on filopodia. Here, by micro-pore based screening, we identify espin as an active regulator for confined migration and cancer metastasis. Espin does not affect random 2D cell motility but enhances confined migration by inducing filopodia formation, along the cell periphery and towards the dorsal surface. Using the imaging-compatible confined microchannels and DNA-based tension probes, we uncover that espin overexpressing cells form excessive filopodia at the leading edge and along the sides, exerting force for confined migration. Overall, these results demonstrate an important role for filopodia and the regulating proteins, such as espin, in confined migration and cancer metastasis.

SUBMITTER: Yan Wang

PROVIDER: S-SCDT-10_1038-S44319-025-00437-1 | biostudies-other |

REPOSITORIES: biostudies-other

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