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DEPDC1B is a key regulator of myoblast proliferation in mouse and man

Nicolas Figeac1, Johanna Pruller1, Isabella Hofer1

  • 1King's College London, Randall Centre for Cell and Molecular Biophysics, London, UK.

Cell Proliferation
|December 12, 2019
PubMed
Abstract

Insights

DISHEVELLED, EGL-10, PLECKSTRIN (DEP) domain-containing 1B (DEPDC1B) drives myoblast proliferation and prevents premature differentiation during skeletal muscle development. Its knockdown inhibits proliferation and promotes differentiation in both mouse and human cells.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Molecular Biology

Background:

  • DISHEVELLED, EGL-10, PLECKSTRIN (DEP) domain-containing 1B (DEPDC1B) is implicated in cell cycle progression and focal adhesion dynamics.
  • DEPDC1B overexpression in cancers correlates with poor patient survival.
  • The role of DEPDC1B in skeletal myogenesis is not well understood.

Purpose of the Study:

  • To investigate the function of DEPDC1B in murine and human skeletal myogenesis.
  • To determine the molecular mechanisms by which DEPDC1B regulates myoblast behavior.

Main Methods:

  • Expression analysis of DEPDC1B in myoblasts and rhabdomyosarcoma cells using RT-qPCR and immunolabelling.
  • Functional studies involving siRNA-mediated knockdown of DEPDC1B, RHOA, and beta-catenin.
  • Analysis of cell cycle regulators and myogenic differentiation markers.

Main Results:

  • DEPDC1B expression is high in proliferating myoblasts and decreases during differentiation.
  • DEPDC1B knockdown reduces myoblast proliferation and accelerates myogenic differentiation.
  • DEPDC1B functions independently of canonical WNT signaling and RHOA in myogenesis, with RHOA knockdown having an additive effect on proliferation reduction and differentiation enhancement.
  • DEPDC1B knockdown promotes myogenic differentiation in rhabdomyosarcoma cells without affecting proliferation.

Conclusions:

  • DEPDC1B is a key regulator of skeletal myogenesis, promoting proliferation and inhibiting premature differentiation.
  • DEPDC1B's role in myogenesis is independent of WNT signaling and RHOA.
  • Targeting DEPDC1B may offer therapeutic potential in muscle-related disorders and cancers.
Keywords:
DEPDC1BRHOAcell proliferationhuman myoblastsrhabdomyosarcomasatellite cells

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