The CDK4/6 Inhibitor Palbociclib Synergizes with ATRA to Induce Differentiation in AML.
Zhimin ZhaiQian LiJiyu WangHuiping WangXiyang RenKeke HuangYangyang WangXue LiangLian-Fang PuShu-Dao XiongZhimin ZhaiPublished in: Molecular cancer therapeutics (2024)
Differentiation therapy based on ATRA almost cured acute promyelocytic leukemia (APL). However, it is disappointing that ATRA is not effective against other acute myeloid leukemia (AML) subtypes. Developing new and effective anti-AML therapies that promote leukemia differentiation is necessary. The CDK4/6-cyclin D pathway is a key initiator of the G1-S phase transition, which determines cell fate. Herein, we investigated whether the CDK4/6 inhibitor palbociclib would synergize with ATRA to promote leukemia differentiation in vitro and in vivo. Our findings revealed that CDK4/6-cyclin D pathway genes were aberrantly expressed in AML, and we observed that palbociclib sensitized AML cells to ATRA-induced morphologic, biochemical, and functional changes indicative of myeloid differentiation. The combination of palbociclib and ATRA attenuated AML cell expansion in vivo. These enhanced differentiation effects may be associated with the regulation of transcription factors, including RARα, E2F1, and STAT1. Overall, our findings demonstrate that CDK4/6 inhibition sensitizes AML cells to ATRA and could guide the development of novel therapeutic strategies for patients with AML.
Keyphrases
- acute myeloid leukemia
- cell cycle
- allogeneic hematopoietic stem cell transplantation
- induced apoptosis
- cell cycle arrest
- cell proliferation
- single cell
- metastatic breast cancer
- signaling pathway
- intensive care unit
- genome wide
- drug induced
- dna methylation
- cell therapy
- immune response
- mass spectrometry
- mesenchymal stem cells
- acute respiratory distress syndrome
- endothelial cells