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Tenofovir Alafenamide Promotes Differentiation and Induces Apoptosis of AML Cells by Inhibiting Telomerase Reverse

Ji-Eun Lee1, Byeol-Eun Jeon1, Chan-Seong Kwon1

  • 1Department of Integrated Biological science, Pusan National University, Busan, Republic of Korea.

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Tenofovir alafenamide (TAF) shows promise as a novel treatment for acute myeloid leukemia (AML). This drug promotes AML cell differentiation and inhibits proliferation, offering a potential new therapeutic strategy for this common adult cancer.

Keywords:
Acute myeloid leukemiaanti-leukemia activitiesdifferentiationdifferentiation therapyreactive oxygen speciestelomerase reverse transcriptasetenofovir alafenamide

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Area of Science:

  • Hematology
  • Oncology
  • Pharmacology

Background:

  • Acute myeloid leukemia (AML) is the most common leukemia in adults, with poor patient prognosis despite advances in understanding its pathogenesis.
  • Current differentiation therapy is effective only for specific AML subtypes, highlighting the need for novel therapeutic agents.

Purpose of the Study:

  • To identify novel therapeutic candidates for AML by screening FDA-approved drugs.
  • To evaluate the anti-leukemia effects and mechanisms of tenofovir alafenamide (TAF) in AML.

Main Methods:

  • Screened 100 FDA-approved drugs for CD11b expression to identify potential candidates.
  • Assessed TAF's effects on AML cell lines (U937, THP-1) using flow cytometry, MTS assays, proliferation assays, and trypan blue staining.
  • Analyzed gene expression, telomere length, and DNA-damage response proteins via real-time PCR and Western blotting.

Main Results:

  • TAF demonstrated significant differentiation-inducing activity in AML cells, reducing viability and proliferation.
  • TAF showed synergistic effects with cytarabine and suppressed proliferation in primary AML samples.
  • TAF inhibited telomerase reverse transcriptase activity, increased reactive oxygen species, and activated the DNA-damage response.

Conclusions:

  • TAF exhibits potent anti-leukemia effects, including differentiation induction and proliferation inhibition.
  • TAF's mechanism involves telomerase inhibition and DNA-damage response activation.
  • TAF represents a promising novel therapeutic agent for AML treatment.