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The non-canonical functions of p27(Kip1) in normal and tumor biology

Savitha S Sharma1, W Jackson Pledger1,2

  • 1a Gibbs Cancer Center & Research Institute , Spartanburg , SC , USA.

Cell Cycle (Georgetown, Tex.)
|April 16, 2016
PubMed

Insights

The protein p27(Kip1), initially known for inhibiting cell proliferation, also has non-canonical functions. These CDK-independent roles can promote or suppress tumors, influencing cancer aggressiveness and metastasis.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • p27(Kip1) is a key regulator of cell proliferation, primarily known for inhibiting cyclin-dependent kinase (CDK) activity.
  • Beyond its canonical role, p27(Kip1) exhibits intrinsically unstructured, multifunctional properties with significant CDK-independent activities.
  • These non-canonical functions impact critical cellular processes including cell cycle, migration, and stem cell behavior.

Purpose of the Study:

  • To review the diverse non-canonical, CDK-independent functions of p27(Kip1).
  • To elucidate the dual role of p27(Kip1) as either a tumor-suppressor or tumor-promoter.
  • To discuss how cell-specific contexts and oncogenic signaling influence p27(Kip1)'s oncogenic potential.

Main Methods:

  • Literature review of studies on p27(Kip1) functions.
  • Analysis of CDK-dependent and CDK-independent mechanisms.
  • Examination of p27(Kip1)'s role in various cellular processes and cancer contexts.

Main Results:

  • p27(Kip1) possesses numerous non-canonical functions independent of CDK inhibition.
  • These functions influence cell cycle, cytoskeletal dynamics, cell migration, and stem cell differentiation.
  • Context-dependent activation of signaling pathways can render p27(Kip1)'s non-canonical functions pro-oncogenic, affecting tumor aggressiveness and metastasis.

Conclusions:

  • p27(Kip1) displays a complex, dual role in cancer, acting as both a tumor suppressor and promoter.
  • Its non-canonical, CDK-independent functions are critical in determining its overall impact on tumorigenesis.
  • Understanding these diverse mechanisms is crucial for developing targeted cancer therapies.
Keywords:
cell cyclecell migrationcyclin-dependent kinasesmetastasisnon-canonical functionsp27Kip1stem-cell biology

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