摘要：SummaryAt the initial stage of carcinogenesis, cell competition often occurs between newly emerging transformed cells and the neighboring normal cells, leading to the elimination of transformed cells from the epithelial layer. For instance, when RasV12-transformed cells are surrounded by normal cells, RasV12 cells are apically extruded from the epithelium. However, the underlying mechanisms of this tumor-suppressive process still remain enigmatic. We first show by electron microscopic analysis that characteristic finger-like membrane protrusions are projected from both normal and RasV12 cells at their interface. In addition, FBP17, a member of the F-BAR proteins, accumulates in RasV12 cells, as well as surrounding normal cells, which plays a positive role in the formation of finger-like protrusions and apical elimination of RasV12 cells. Furthermore, cdc42 acts upstream of these processes. These results suggest that the cdc42/FBP17 pathway is a crucial trigger of cell competition, inducing “protrusion to protrusion response” between normal and RasV12-transformed cells.Graphical abstractDisplay OmittedHighlights•EM analysis shows finger-like membrane protrusions between normal and RasV12 cells•Cdc42/FBP17 regulate the formation of the finger-like membrane protrusions•Cdc42/FBP17-mediated finger-like protrusions promote elimination of RasV12 cells•‘Protrusion to protrusion response’ triggers cell competitionOptics; Cell biology; Organizational aspects of cell biology
