Authors

Silvia Pomella, IRCCS Ospedale Pediatrico Bambino Gesù
Matteo Cassandri, IRCCS Ospedale Pediatrico Bambino Gesù
Lucrezia D’Archivio, IRCCS Ospedale Pediatrico Bambino Gesù
Antonella Porrazzo, IRCCS Ospedale Pediatrico Bambino Gesù
Cristina Cossetti, IRCCS Ospedale Pediatrico Bambino Gesù
Doris Phelps, University of Texas Health Science Center at San Antonio
Clara Perrone, IRCCS Ospedale Pediatrico Bambino Gesù
Michele Pezzella, IRCCS Ospedale Pediatrico Bambino Gesù
Antonella Cardinale, IRCCS Ospedale Pediatrico Bambino Gesù
Marco Wachtel, Kinderspital Zürich
Sara Aloisi, Case Western Reserve University
David Milewski, National Cancer Institute (NCI)
Marta Colletti, IRCCS Ospedale Pediatrico Bambino Gesù
Prethish Sreenivas, University of Texas Health Science Center at San Antonio
Zoë S. Walters, The Institute of Cancer Research
Giovanni Barillari, Università degli Studi di Roma "Tor Vergata"
Angela Di Giannatale, IRCCS Ospedale Pediatrico Bambino Gesù
Giuseppe Maria Milano, IRCCS Ospedale Pediatrico Bambino Gesù
Cristiano De Stefanis, IRCCS Ospedale Pediatrico Bambino Gesù
Rita Alaggio, IRCCS Ospedale Pediatrico Bambino Gesù
Sonia Rodriguez-Rodriguez, City of Hope National Med Center
Nadia Carlesso, City of Hope National Med Center
Christopher R. Vakoc, Cold Spring Harbor Laboratory
Enrico Velardi, IRCCS Ospedale Pediatrico Bambino Gesù
Beat W. Schafer, Kinderspital Zürich
Ernesto Guccione, Icahn School of Medicine at Mount Sinai
Susanne A. Gatz, University of Birmingham
Lucio Miele, LSU Health Sciences Center - New OrleansFollow

Document Type

Article

Publication Date

12-15-2023

Publication Title

Nature Communications

Abstract

Rhabdomyosarcomas (RMS) are pediatric mesenchymal-derived malignancies encompassing PAX3/7-FOXO1 Fusion Positive (FP)-RMS, and Fusion Negative (FN)-RMS with frequent RAS pathway mutations. RMS express the master myogenic transcription factor MYOD that, whilst essential for survival, cannot support differentiation. Here we discover SKP2, an oncogenic E3-ubiquitin ligase, as a critical pro-tumorigenic driver in FN-RMS. We show that SKP2 is overexpressed in RMS through the binding of MYOD to an intronic enhancer. SKP2 in FN-RMS promotes cell cycle progression and prevents differentiation by directly targeting p27Kip1 and p57Kip2, respectively. SKP2 depletion unlocks a partly MYOD-dependent myogenic transcriptional program and strongly affects stemness and tumorigenic features and prevents in vivo tumor growth. These effects are mirrored by the investigational NEDDylation inhibitor MLN4924. Results demonstrate a crucial crosstalk between transcriptional and post-translational mechanisms through the MYOD-SKP2 axis that contributes to tumorigenesis in FN-RMS. Finally, NEDDylation inhibition is identified as a potential therapeutic vulnerability in FN-RMS.

PubMed ID

38102140

Volume

14

Issue

1

Comments

See article for full author list.

Creative Commons License

Creative Commons Attribution 4.0 International License
This work is licensed under a Creative Commons Attribution 4.0 International License.

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