The HDAC3–SMARCA4–miR-27a axis promotes expression of the <i>PAX3:FOXO1</i> fusion oncogene in rhabdomyosarcoma
Narendra Bharathy(Children's Cancer Therapy Development Institute), Noah Berlow(Children's Cancer Therapy Development Institute), Eric Wang(Cold Spring Harbor Laboratory), Jinu Abraham(Oregon Health & Science University), Teagan P. Settelmeyer(Children's Cancer Therapy Development Institute), Jody E. Hooper(Johns Hopkins University), Matthew N. Svalina(Children's Cancer Therapy Development Institute), Yoshihiro Ishikawa(Shriners Hospitals for Children - Portland), Keith Zientek(Shriners Hospitals for Children - Portland), Zia Bajwa(Oregon Health & Science University), Martin Goros(The University of Texas at San Antonio Health Science Center), Brian Hernandez(The University of Texas at San Antonio Health Science Center), Johannes Wolff(Cleveland Clinic), Michelle A. Rudek(Johns Hopkins University), Linping Xu(Johns Hopkins University), Nicole M. Anders(Johns Hopkins University), Ranadip Pal(Texas Tech University), Alexandria P. Harrold(Children's Cancer Therapy Development Institute), Angela M. Davies(Champions Oncology (United States)), Arya Ashok(Champions Oncology (United States)), Darnell Bushby(Champions Oncology (United States)), Maria Mancini(Champions Oncology (United States)), Christopher Noakes(Champions Oncology (United States)), Neal Goodwin(Champions Oncology (United States)), Peter Ordentlich, James Keck(Jackson Laboratory), Douglas S. Hawkins(Seattle Children's Hospital), Erin R. Rudzinski(Seattle Children's Hospital), Bishwanath Chatterjee(National Cancer Institute), Hans Peter Bächinger(Oregon Health & Science University), Frederic G. Barr(National Cancer Institute), Jennifer Liddle(University of Pennsylvania), Benjamin A. García(University of Pennsylvania), Atiya Mansoor(Oregon Health & Science University), Theodore J. Perkins(University of Ottawa), Christopher R. Vakoc(Cold Spring Harbor Laboratory), Joel Michalek(The University of Texas at San Antonio Health Science Center), Charles Keller(Children's Cancer Therapy Development Institute)
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Abstract
mRNA destabilization and chemotherapy sensitization in aRMS cells in culture and in vivo. Furthermore, a phase 1 clinical trial (ADVL1513) has shown that entinostat is tolerable in children with relapsed or refractory solid tumors and is planned for phase 1B cohort expansion or phase 2 clinical trials. Together, these results implicate an HDAC3-SMARCA4-miR-27a-PAX3:FOXO1 circuit as a driver of chemoresistant aRMS and suggest that targeting this pathway with entinostat may be therapeutically effective in patients.
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