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p27kip1 controls cell morphology and motility by regulating microtubule-dependent lipid raft recycling

Barbara Belletti1, Ilenia Pellizzari, Stefania Berton

  • 1Division of Experimental Oncology 2, Centro di Riferimento Oncologico, National Cancer Institute, Via Franco Gallini, 2, 33081 Aviano, Italy.

Molecular and Cellular Biology
|March 3, 2010
PubMed

Insights

The protein p27(kip1) (p27) stabilizes microtubules (MTs) and influences cell migration. Loss of p27 alters cell shape and motility in 3D environments, a phenotype reversed by stathmin ablation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • p27(kip1) (p27) inhibits cyclin/cyclin-dependent kinase complexes and its nuclear loss correlates with poor prognosis in solid tumors.
  • Cytoplasmic p27 binds Op18/stathmin (stathmin), a microtubule-destabilizing protein, to stabilize microtubules (MTs) and inhibit cell migration.

Purpose of the Study:

  • To investigate the role of p27 in regulating cell morphology, motility, and microtubule stability within three-dimensional (3D) matrices.
  • To elucidate the functional relationship between p27 and stathmin in controlling cytoskeletal organization and cell behavior in 3D environments.

Main Methods:

  • Utilized p27 null cells and Stathmin-ablated cells in 3D matrix cultures.
  • Analyzed cell morphology, motility modes (mesenchymal-amoeboid conversion), microtubule (MT) stability, lipid raft trafficking, and RhoA activity.
  • Investigated the rescue effect of Stathmin genetic ablation on p27 null cell phenotypes.

Main Results:

  • p27 null cells exhibited decreased MT stability, a rounded morphology in 3D, and a shift towards amoeboid motility.
  • Loss of p27 led to accelerated lipid raft trafficking and increased RhoA activity upon cell-extracellular matrix contact.
  • Concomitant genetic ablation of Stathmin rescued the altered cell morphology, motility, and MT network characteristics in p27 null cells.

Conclusions:

  • The p27-stathmin interaction is critical for maintaining cytoskeletal organization and normal cell behavior in 3D environments.
  • Balanced expression of p27 and stathmin is a key determinant of cell morphology, MT stability, and motility in 3D contexts.
  • Targeting the p27-stathmin pathway may offer therapeutic strategies for solid tumors by modulating cell migration and invasion.

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