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PKC Dependent p14ARF Phosphorylation on Threonine 8 Drives Cell Proliferation

Rosa Fontana1, Daniela Guidone1, Felicia Sangermano1

  • 1Department of Biology, Università degli Studi di Napoli "Federico II", Napoli, Italy.

Scientific Reports
|May 6, 2018
PubMed

Insights

ARF protein

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oncology

Background:

  • The tumor suppressor role of ARF is context-dependent.
  • ARF loss in HeLa cells causes cell spreading defects, reduced phosphorylated Focal Adhesion Kinase (FAK), and anoikis.
  • PKC-dependent signaling stabilizes ARF.

Purpose of the Study:

  • To investigate the role of ARF phosphorylation in cell proliferation.
  • To determine if ARF phosphorylation regulates cell spreading and FAK activation.
  • To explore the implications of ARF phosphorylation in cancer.

Main Methods:

  • Utilized HeLa cells and ARF mutants.
  • Investigated ARF induction via PKC activation during cell spreading.
  • Analyzed the effects of a constitutively phosphorylated ARF mutant (T8D) on cell spreading, FAK activation, and cell growth.

Main Results:

  • ARF is induced upon cell spreading through PKC activation.
  • A constitutively phosphorylated ARF mutant (T8D) promotes cell spreading and FAK activation.
  • Expression of ARF-T8D confers a growth advantage to cells.

Conclusions:

  • ARF phosphorylation, particularly at T8, is a key regulator of cell spreading and FAK activation.
  • ARF phosphorylation may act as a signaling mechanism for pro- or anti-proliferative signals in physiological and pathological contexts.
  • This highlights a novel mechanism for ARF's context-dependent functions in cell growth and potentially cancer.

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