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Interleukin-24 (IL24) Is Suppressed by PAX3-FOXO1 and Is a Novel Therapy for Rhabdomyosarcoma

Alexandra Lacey1, Erik Hedrick1, Yating Cheng1

  • 1Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Texas.

Molecular Cancer Therapeutics
|September 8, 2018
PubMed

Insights

Alveolar rhabdomyosarcoma (ARMS) is driven by PAX3-FOXO1, which suppresses the tumor suppressor IL24. Restoring IL24 inhibits ARMS growth, offering a potential new therapy for patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Alveolar rhabdomyosarcoma (ARMS) is characterized by poor prognosis, largely due to the oncogenic fusion protein PAX3-FOXO1.
  • PAX3-FOXO1 overexpression is linked to repressed interleukin-24 (IL24) expression in ARMS tumors, showing an inverse relationship.

Purpose of the Study:

  • To investigate the regulatory relationship between PAX3-FOXO1 and IL24 in ARMS.
  • To evaluate the therapeutic potential of IL24 in ARMS models.

Main Methods:

  • RNA-sequencing and RNA interference studies were employed to analyze gene expression and functional impacts.
  • In vivo studies involved direct injection of adenoviral-expressed IL24 into ARMS tumors in mice.

Main Results:

  • PAX3-FOXO1 represses IL24 expression in an HDAC5-dependent manner.
  • Knockdown of PAX3-FOXO1 or overexpression of IL24 inhibited ARMS cell proliferation, survival, and migration.
  • IL24 restoration significantly reversed the effects of PAX3-FOXO1 knockdown.
  • Adenoviral IL24 administration reduced tumor growth and weight in vivo.

Conclusions:

  • IL24 acts as a tumor suppressor in ARMS and its restoration can inhibit tumor progression.
  • Adenoviral IL24 represents a promising therapeutic strategy for ARMS, with potential for use alone or in combination therapies.

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