ArticleCell death & disease2026
Inhibition of Pellino-1 reverts the progression and tyrosine kinase inhibitor resistance in chronic myeloid leukemia.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BCR-ABL1, derived from structural chromosome rearrangements, is the driver mutation in chronic myeloid leukemia (CML). Targeting BCR-ABL1 for degradation is an ideal therapeutic strategy for CML, however, the regulatory mechanisms controlling BCR-ABL1 expression in CML remained unclear. Here, we identified PELI1 as a key regulator for maintaining BCR-ABL1 in CML. BCR-ABL1 upregulates PELI1 via the STAT5/FOXP3 pathway, and the increased PELI1 then interacts with and protects BCR-ABL1 from degradation in CML cells. Concurrently, PELI1 functions as a downstream effector to promote CML cell proliferation. Notably, genetic or pharmacological inhibition of PELI1 effectively suppresses the proliferation of both tyrosine kinase inhibitors (TKIs)-sensitive and TKI-resistant CML cells, as well as Leukemia stem cells (LSCs), which consequently ameliorates the disease burden and progression of CML. Collectively, our findings demonstrated that targeting PELI1 is a promising therapeutic strategy for CML that can overcome TKI resistance and eliminates LSCs.
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