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June 15, 2026Cell Death and Disease0 citationsOpen Access

Core transcriptional regulatory circuitry identified from patient-derived tumor cells provides a specific vulnerability for rhabdomyosarcoma

SLS L LiuZHZiqi HeXCXue Chen

Key Points

  • The study aims to identify core transcriptional regulatory circuitry in rhabdomyosarcoma and its role in tumor maintenance.
  • Established 15 patient-derived tumor cells from RMS specimens.
  • Conducted CUT&Tag-seq for H3K27ac to identify super-enhancers and associated genes.
  • Utilized CDK7 inhibition by THZ1 to assess effects on tumor cell proliferation.
  • Knockdown of SMAD3, RUNX2, JUN, and FOS reduced CRC member expression and inhibited tumor growth.
  • CDK7 inhibition with THZ1 significantly suppressed cell proliferation in RMS.
  • The identified CRC represents a crucial vulnerability for targeted therapy in RMS.

Abstract

Abstract Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma in children and adolescents, with limited targeted treatment options. Core transcriptional regulatory circuitry (CRC) proteins play crucial roles in tumor cell identity and survival. Here, we established 15 patient-derived tumor cells (PDCs) from RMS specimens and found that these cells retained the expression of RMS hallmark and dependency genes, as well as the genetic mutations in primary tumors. Cleavage under targets and tagmentation sequencing (CUT&Tag-seq) for H3K27ac in these RMS PDCs identified super-enhancers and the associated CRC, which contained SMAD3, RUNX2, JUN and FOS. These factors formed an interconnected auto-regulatory loop that maintained the malignant cell state in RMS. Knocking down each of these genes decreased the expression of all the CRC members and impaired tumor cell growth in RMS. CDK7 inhibition by THZ1 disrupted the CRC and effectively suppressed cell proliferation in RMS. Our study demonstrates a common CRC in RMS that is essential for tumor maintenance, providing a promising therapeutic vulnerability for RMS.

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Cite This Study

Liu et al. (2026) studied this question.

synapsesocial.com/papers/6a2f984ba1cfeec4908293fchttps://doi.org/10.1038/s41419-026-08949-x
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Abstract 3500: Synergistic targeting of EP300/CBP and EYA co-activators collapses the rhabdomyosarcoma core regulatory circuit2026
  2. 2Abstract A001: PAX3-FOXO1-induced transcriptional dysregulation in rhabdomyosarcoma2024
  3. 3Abstract B015: CDK12 pharmacological targeting promotes cell death by abrogating DNA damage response, impairs PAX3-FOXO1 expression and synergizes with BRD4 and PARP inhibitors in fusion positive rhabdomyosarcoma2025
  4. 4Abstract 136: Determining the genomic basis of PAX3-FOXO1 mediated transformation in rhabdomyosarcoma2024
  5. 5Single cell transcriptomic profiling identifies tumor-acquired and therapy-resistant cell states in pediatric rhabdomyosarcoma2024 · 41 citations