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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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Cell crowding triggers cell death through caspase activation and delamination, independent of fitness. This mechanical super-competition may drive tumor growth.

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Area of Science:

  • Developmental Biology
  • Cell Biology
  • Biophysics

Background:

  • Tissue size regulation involves cell proliferation, volume, and death.
  • Cell death's role in tissue scaling is less understood than growth.
  • Epithelial cell elimination via delamination was recently observed in response to cell density.

Purpose of the Study:

  • Investigate the mechanisms of cell elimination in Drosophila pupal notum.
  • Clarify the role of caspase activation in cell delamination.
  • Determine if tissue crowding drives cell elimination independently of fitness-based competition.

Main Methods:

  • Live-cell delamination studies in Drosophila pupal notum.
  • Caspase 3 activation assays.
  • Particle image velocimetry, genetics, and laser-induced perturbations.
  • Ras oncogene activation in clones.

Main Results:

  • Caspase 3 activation precedes and is required for cell delamination.
  • Local tissue crowding is necessary and sufficient for cell elimination.
  • Cell elimination occurs independently of known fitness-dependent competition pathways.
  • Ras activation induces tissue compression and eliminates neighboring cells.

Conclusions:

  • Crowding-induced cell death is mediated by caspase activation and delamination.
  • This represents a novel form of 'mechanical super-competition'.
  • Mechanical super-competition is independent of fitness markers and could contribute to tumor growth.