A novel DAG-dependent mechanism links PKCa and Cyclin B1 regulating cell cycle progression

Alessandro Poli, Giulia Ramazzotti, Alessandro Matteucci, Lucia Manzoli, Annalisa Lonetti, Pann Ghill Suh, James A. McCubrey, Lucio Cocco

Research output: Contribution to journalArticlepeer-review

Abstract

Through the years, different studies showed the involvement of Protein Kinase C (PKC) in cell cycle control, in particular during G1/S transition. Little is known about their role at G2/M checkpoint. In this study, using K562 human erythroleukemia cell line, we found a novel and specific mechanism through which the conventional isoform PKCa positively affects Cyclin B1 modulating G2/M progression of cell cycle. Since the kinase activity of this PKC isoform was not necessary in this process, we demonstrated that PKCa, physically interacting with Cyclin B1, avoided its degradation and stimulated its nuclear import at mitosis. Moreover, the process resulted to be strictly connected with the increase in nuclear diacylglycerol levels (DAG) at G2/M checkpoint, due to the activity of nuclear Phospholipase C β1 (PLCβ1), the only PLC isoform mainly localized in the nucleus of K562 cells. Taken together, our findings indicated a novel DAG dependent mechanism able to regulate the G2/M progression of the cell cycle.

Original languageEnglish
Pages (from-to)11526-11540
Number of pages15
JournalOncotarget
Volume5
Issue number22
Publication statusPublished - 2014

Keywords

  • Cell cycle
  • Cyclin
  • DAG
  • Nuclei
  • PKC
  • PLC

ASJC Scopus subject areas

  • Oncology

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