ArticleJournal of molecular cell biology2024
Loss of the vitamin D receptor triggers senescence in chronic myeloid leukemia via DDIT4-mediated DNA damage.
Article in Journal of molecular cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Exploiting cellular senescence in hematologic malignancies.Translational oncology · 2026Review
- Identification of Cellular Senescence-Related Critical Genes and Molecular Classification and Revealing the Drug-Resistant Therapeutic Effect of IGFBP2 in Chronic Myeloid Leukemia.Journal of inflammation research · 2024Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Chronic myeloid leukemia (CML) is a hematopoietic malignancy driven by the fusion gene BCR::ABL1. Drug resistance to tyrosine kinase inhibitors (TKIs), due to BCR::ABL1 mutations and residual leukemia stem cells (LSCs), remains a major challenge in CML treatment. Here, we revealed the requirement of the vitamin D receptor (VDR) in the progression of CML. VDR was upregulated by BCR::ABL1 and highly expressed in CML cells. Interestingly, VDR knockdown inhibited the proliferation of CML cells driven by both BCR::ABL1 and TKI-resistant BCR::ABL1 mutations. Mechanistically, VDR transcriptionally regulated DDIT4 expression; reduced DDIT4 levels upon VDR knockdown triggered DNA damage and senescence via p53 signaling activation in CML cells. Furthermore, VDR deficiency not only suppressed tumor burden and progression in primary CML mice but also reduced the self-renewal capacity of CML-LSCs. Together, our study demonstrated that targeting VDR is a promising strategy to overcome TKI resistance and eradicate LSCs in CML.
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Registered trials
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