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The RNA m6A Reader YTHDF1 Is Required for Acute Myeloid Leukemia Progression.

Yun-Guang Hong1, Zhigang Yang1,2,3, Yan Chen1

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YTHDF1, an m6A reader, drives acute myelogenous leukemia (AML) progression by boosting cyclin E2 translation. The FDA-approved drug tegaserod inhibits YTHDF1, suppressing AML growth and improving survival in models.

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Area of Science:

  • Molecular Biology
  • Oncology
  • RNA Modifications

Background:

  • N6-methyladenosine (m6A) is the most abundant mRNA modification and plays a key role in acute myelogenous leukemia (AML) pathogenesis.
  • Identifying regulators of m6A in AML is crucial for understanding disease biology and developing novel therapeutic strategies.

Purpose of the Study:

  • To investigate the role of the m6A reader protein YTHDF1 in AML.
  • To identify potential therapeutic strategies targeting YTHDF1 in AML.

Main Methods:

  • Overexpression of YTHDF1 in human AML samples and leukemia stem cells (LSCs) was assessed.
  • YTHDF1's function in AML cell proliferation, self-renewal, and leukemic capacity was evaluated in vitro and in vivo.
  • Mechanisms of YTHDF1 action, including its role in cyclin E2 translation, were investigated.
  • FDA-approved drugs were screened for YTHDF1 inhibitory activity, leading to the identification of tegaserod.
  • Tegaserod's effects on YTHDF1 binding, cyclin E2 translation, AML cell viability, and patient-derived xenograft models were examined.

Main Results:

  • YTHDF1 is overexpressed in human AML, particularly in LSCs.
  • Depletion of YTHDF1 impairs AML cell self-renewal, proliferation, and leukemic capacity.
  • YTHDF1 promotes cyclin E2 translation in an m6A-dependent manner.
  • Tegaserod inhibits YTHDF1's interaction with m6A-modified mRNAs and suppresses YTHDF1-driven cyclin E2 translation.
  • Tegaserod reduces the viability of patient-derived AML cells and prolongs survival in xenograft models.

Conclusions:

  • YTHDF1 is a critical regulator of AML progression by controlling the expression of m6A-modified mRNAs.
  • YTHDF1 represents a potential therapeutic target for AML.
  • Tegaserod, an FDA-approved drug, demonstrates potential as a YTHDF1 inhibitor for AML treatment.