Research Papers:

IPMK and β-catenin mediate PLC-β1-dependent signaling in myogenic differentiation

Giulia Ramazzotti, Anna Maria Billi, Lucia Manzoli, Cristina Mazzetti, Alessandra Ruggeri, Christophe Erneux, Seyun Kim, Pann-Ghill Suh, Lucio Cocco and Irene Faenza _

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Oncotarget. 2016; 7:84118-84127. https://doi.org/10.18632/oncotarget.11527

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Giulia Ramazzotti1, Anna Maria Billi1, Lucia Manzoli1, Cristina Mazzetti1, Alessandra Ruggeri1, Christophe Erneux2, Seyun Kim4, Pann-Ghill Suh3, Lucio Cocco1, Irene Faenza1

1Cellular Signalling Laboratory, Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy

2Interdisciplinary Research Institute (IRIBHM), Université Libre de Bruxelles, Campus Erasme, Brussels, Belgium

3Department of Biological Sciences, School of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, Republic of Korea

4Department of Biological Sciences, KAIST, Daejeon, Republic of Korea

Correspondence to:

Lucio Cocco, email: [email protected]

Irene Faenza, email: [email protected]

Keywords: myogenic differentiation, phospholipase C-β1, IPMK, β-catenin, inositol phosphates

Received: June 06, 2016     Accepted: August 15, 2016     Published: August 23, 2016


In previous studies, we have reported that phospholipase C (PLC)-β1 plays a crucial role in myogenic differentiation and we determined the importance of its catalytic activity for the initiation of this process. Here we define the effectors that take part to its signaling pathway. We show that the Inositol Polyphosphate Multikinase (IPMK) is able to promote myogenic differentiation since its overexpression determines the up-regulation of several myogenic markers. Moreover, we demonstrate that IPMK activates the same cyclin D3 promoter region targeted by PLC-β1 and that IPMK-induced promoter activation relies upon c-jun binding to the promoter, as we have shown previously for PLC-β1. Furthermore, our data shows that IPMK overexpression causes an increase in β-catenin translocation and accumulation to the nuclei of differentiating myoblasts resulting in higher MyoD activation. Finally, we describe that PLC-β1 overexpression determines too an increase in β-catenin translocation and that PLC-β1, IPMK and β-catenin are mediators of the same signaling pathway since their overexpression results in cyclin D3 and myosin heavy chain (MYH) induction.

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