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Updated: Nov 22, 2025

Identification of MyoD Interactome Using Tandem Affinity Purification Coupled to Mass Spectrometry
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Interaction between SNAI2 and MYOD enhances oncogenesis and suppresses differentiation in Fusion Negative

Silvia Pomella1,2, Prethish Sreenivas3, Berkley E Gryder2

  • 1Department of Pediatric Hematology and Oncology, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.

Nature Communications
|January 9, 2021
PubMed

Insights

SNAI2 oncogene blocks muscle cell differentiation in pediatric rhabdomyosarcoma (RMS). It interacts with MYOD and RAS signaling, promoting tumor growth and preventing normal muscle development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Developmental Biology

Background:

  • Rhabdomyosarcoma (RMS) is a pediatric muscle cancer.
  • Fusion Positive (FP)-RMS has PAX3/7-FOXO1, Fusion Negative (FN)-RMS often has RAS mutations.
  • RMS cells express myogenic factors but fail terminal differentiation.

Purpose of the Study:

  • Investigate the role of SNAI2 in Fusion Negative Rhabdomyosarcoma.
  • Determine how SNAI2 impacts myogenic differentiation and tumor growth.
  • Elucidate the interplay between SNAI2, MYOD, and RAS signaling in RMS.

Main Methods:

  • Chromatin binding analysis to map SNAI2 and MYOD interactions.
  • Gene expression analysis of myogenic differentiation markers.
  • Assessment of SNAI2 expression in FN-RMS samples.

Main Results:

  • SNAI2 is highly expressed in FN-RMS and promotes tumor growth.
  • SNAI2 blocks myogenic differentiation by competing with MYOD at enhancers.
  • RAS/MEK signaling influences SNAI2 levels and chromatin binding.

Conclusions:

  • SNAI2 is an oncogene that inhibits muscle cell differentiation in RMS.
  • SNAI2, MYOD, and RAS signaling create a differentiation blockade promoting tumorigenesis.
  • Targeting SNAI2 may offer a therapeutic strategy for FN-RMS.

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