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December 8, 2025BloodOpen Access

The long non-coding RNA WT1-AS controls differentiation programs and leukemic cell fate in AML

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Authors

PFPascal FichtelSBSilke Brilloff

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Overview

Knockdown of long non-coding RNA WT1-AS induces apoptosis and cell cycle arrest in AML, suggesting its role as a therapeutic target.

Key Points

  • To explore the role of long non-coding RNA WT1-AS in differentiation programs and leukemic stem cell fate in acute myeloid leukemia (AML).
  • Established WT1-AS knockdown in AML cell lines using shRNA.
  • Performed growth competition assays with RFP-labeling.
  • Analyzed cell cycle properties and apoptosis after WT1-AS knockdown.
  • Conducted transcriptomic analyses to identify gene signature changes.
  • Utilized an AML patient-derived xenograft model to assess the influence of WT1-AS on AML progression.
  • WT1-AS knockdown led to increased apoptosis and cell cycle arrest in the G0/G1 phase.
  • Transcriptomic analyses revealed upregulation of myeloid differentiation gene signatures in WT1-AS knockdown cells.
  • In vivo models showed reduced engraftment of AML cells following WT1-AS knockdown.
  • The cohort with low WT1-AS expression displayed distinct myeloid differentiation gene signatures.

Cite This Study

Fichtel et al. (2025) studied this question.

synapsesocial.com/papers/693624d74fa91c937236d0dehttps://doi.org/10.1182/blood-2025-5022
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