ArticleInternational journal of hematology2021
Inhibition of CDK4/6 and autophagy synergistically induces apoptosis in t(8;21) acute myeloid leukemia cells.
Article in International journal of hematology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- The synergistic tumor suppressor effect of CDK4/6 inhibitors and BRD4 inhibitors in acute myeloid leukemia.Leukemia research reports · 2026Article
- Synergistic potential of CDK4/6 inhibitors and ATRA in non-APL AML.British journal of haematology · 2025Article
- LRRC1 knockdown downregulates MACF1 to inhibit the malignant progression of acute myeloid leukemia by inactivating β-catenin/c-Myc signaling.Journal of molecular histology · 2024Article
- Review
- Potential anticancer properties of calotropis procera: An investigation on breast and colon cancer cells.Heliyon · 2023Article
- A review on the role of cyclin dependent kinases in cancers.Cancer cell international · 2022Review
- The dual role of autophagy in acute myeloid leukemia.Journal of hematology & oncology · 2022Review
- Presence of theFrontiers in oncology · 2022Article
- Cyclin-dependent kinase 6 (CDK6) as a potent regulator of the ovarian primordial-to-primary follicle transition.Frontiers in cell and developmental biology · 2022Article
- Review
- Efficacy of a combination therapy targeting CDK4/6 and autophagy in a mouse xenograft model of t(8;21) acute myeloid leukemia.Biochemistry and biophysics reports · 2021Article
- Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The t(8;21) translocation is the most common cytogenetic abnormality in acute myeloid leukemia (AML). Although t(8;21) AML patients have a relatively favorable prognosis, relapse is a frequent occurrence, underscoring the need to develop novel therapeutic approaches. Here, we showed that t(8;21) AML is characterized by frequent mutation and overexpression of CCND2. Analysis of 19 AML cell lines showed that t(8;21) AML cells had lower IC50 values for the selective CDK4/6 inhibitors palbociclib and abemaciclib than non-t(8;21) AML cells. CDK4/6 inhibitors caused cell cycle arrest at G1 phase and impaired cell proliferation in t(8;21) AML cells. CDK4/6 inhibition decreased MAP-ERK and PI3K-AKT-mTOR signaling pathway activity, induced LC3B-I to LC3B-II conversion, and enhanced autophagosome formation, suggesting autophagy induction. Treatment of t(8;21) AML cells with the autophagy inhibitors chloroquine (CQ) or LY294002 in combination with the CDK4/6 inhibitor abemaciclib significantly increased the percentage of apoptotic (Annexin V positive) cells, whereas CQ or LY294002 single treatment had no significant effects. The effectiveness of co-inhibiting CDK4/6 and autophagy was confirmed in primary t(8;21) AML cells. The results suggest that the combination of CDK4/6 and autophagy inhibitors had a synergistic effect on inducing apoptosis, suggesting a novel therapeutic approach for the treatment of t(8;21) AML.
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