Cyclin dependent kinase 9 (Cdk9) is a member of the cyclin dependent kinase family. The
regulatory units of Cdk9 are the T family Cyclins (T1, T2) and Cyclin K1. Cyclin T2 has two
forms termed CycT2a and CycT2b that arise by an alternative splicing of the primary transcript.
Previous studies underscored a crucial role for Cdk9 in association of Cyclin T2 during skeletal
myogenesis. Upon induction of muscle differentiation, MyoD recruits Cdk9/CycT2 on musclespecific
gene promoter sequences. This complex is able to phosphorylate the C-terminal domain
of RNA polymerase II, enhancing Myod function and promoting myogenic differentiation.
Rhabdomyosarcoma (RMS), one of the most common childhood solid tumor, arises from muscle
precursor cells and fails to complete both the differentiation program both the irreversibly cell
cycle exit, resulting in uncontrolled proliferation and incomplete myogenesis. In RMS, Cdk9
fails to phosphorylate MyoD and the ability of MyoD to arrest cell proliferation and to activate
the myogenic program is repressed. The result of this study confirmed the involvement of Cdk9/
CyclinT2 complexes during the myogenesis. Both isoforms of Cyclin T2 are able to activate the
myogenic program at different stages of differentiation but CycT2b have a predominant role of
in particular during the latest stages. Moreover we demonstred that EZH2 is probably responsible
to inhibition of Cdk9 in RMS cells and her overexpression contribuite to inhibition of
myogenesis
