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RUNX1 transactivates BCR-ABL1 expression in Philadelphia chromosome positive acute lymphoblastic leukemia.

Tatsuya Masuda1, Shintaro Maeda1, Sae Shimada1

  • 1Department of Human Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Cancer Science
|December 13, 2021
PubMed
Summary

A novel RUNX inhibitor, Chb-M

Keywords:
Philadelphia chromosomeRUNX1 protein, humanbcr-ablfusion proteinsgene expression regulationleukemialymphoid

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Area of Science:

  • Hematology
  • Molecular Biology
  • Oncology

Background:

  • Tyrosine kinase inhibitors (TKIs) have improved outcomes for Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL).
  • TKI resistance, often due to BCR-ABL1 mutations, necessitates new therapeutic strategies for Ph+ ALL.
  • Identifying novel targets is crucial for overcoming TKI resistance in Ph+ ALL.

Purpose of the Study:

  • To investigate the role of RUNX1 transcription factor in BCR-ABL1 expression in Ph+ ALL.
  • To evaluate the efficacy of a novel RUNX inhibitor, Chb-M', in targeting TKI-resistant Ph+ ALL.
  • To explore Chb-M' as a therapeutic strategy for overcoming TKI resistance in Ph+ ALL.

Main Methods:

  • In vitro studies using Ph+ ALL cell lines to assess RUNX1 binding to the BCR promoter.
  • RUNX1 knockdown experiments to evaluate effects on BCR-ABL1 expression and cell proliferation.
  • Treatment of Ph+ ALL cell lines, including imatinib-resistant lines, with Chb-M'.
  • In vivo experiments using patient-derived xenograft models of Ph+ ALL.

Main Results:

  • RUNX1 directly transactivates BCR-ABL1 expression in Ph+ ALL cell lines.
  • RUNX1 knockdown reduced BCR-ABL1 expression and suppressed proliferation.
  • Chb-M' treatment downregulated BCR-ABL1 expression and showed efficacy in imatinib-resistant Ph+ ALL cells.
  • In vivo studies corroborated the in vitro findings.

Conclusions:

  • RUNX1 plays a critical role in regulating BCR-ABL1 expression in Ph+ ALL.
  • Targeting RUNX1 with Chb-M' represents a promising strategy to overcome TKI resistance in Ph+ ALL.
  • Chb-M' demonstrates potential as a novel therapeutic agent for TKI-resistant refractory Ph+ ALL.