Anticancer agent FTY720 upregulates cell cycle regulator BTG2 via the SET/TAF-Iβ –PP2A–SMAD3 signaling pathway and induces G2/M arrest in leukemia

Key Points

• G2/M arrest occurs following the upregulation of the cell cycle regulator BTG2.
• FTY720 treatment resulted in significant modulation of the SET/TAF-Iβ – PP2A – SMAD3 signaling pathway.
• The intervention highlights the potential of targeting this signaling pathway in leukemia therapies.
• Further investigation is needed to explore the full therapeutic implications of FTY720 in clinical settings.