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

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)

Lucio Cocco (Creator)

Annalisa Lonetti (Creator)

Lucia Manzoli (Creator)

Alessandro Matteucci (Creator)

James A. McCubrey (Creator)

Alessandro Poli (Creator)

Giulia Ramazzotti (Creator)

Pann-Ghill Suh (Creator)

Institution

East Carolina University (ECU )

Web Site: http://www.ecu.edu/lib/

Abstract: Extracted text; 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 PKC? 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 PKC?, 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 ß1 (PLCß1), 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.

Additional Information

Publication

Other

Oncotarget; 5:22 p. 11526-11540

Language: English

Date: 2014

Keywords

PLC, DAG, nuclei, PKC, Cyclin, Cell Cycle

Email this document to