ArticleJournal of hematology & oncology2017
Inhibition of LIN28B impairs leukemia cell growth and metabolism in acute myeloid leukemia.
Article in Journal of hematology & oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 75 citations in OpenAlex.
- Ribosomal protein control of hematopoietic stem cell transformation through regulation of metabolism.Cell reports · 2025Article
- Recent advances in drug delivery and treatment strategies for acute myeloid leukemia.International journal of pharmaceutics · 2025Review
- Let-7 Family microRNAs Regulate the Expression of the Urokinase-Receptor in Acute Myeloid Leukemia Cells.Cells · 2025Article
- Norchelerythrine fromInternational journal of oncology · 2025Article
- NMolecular medicine (Cambridge, Mass.) · 2024Review
- Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) in hematological diseases.Molecular medicine (Cambridge, Mass.) · 2024Review
- Review
- Evaluation of Clinically Significant miRNAs Level by Machine Learning Approaches Utilizing Total Transcriptome Data.Doklady. Biochemistry and biophysics · 2024Article
- Transcriptional repression of the oncofetal LIN28B gene by the transcription factor SOX6.Scientific reports · 2024Article
- A Multi-Omics Approach Reveals Enrichment in Metabolites Involved in the Regulation of the Glutathione Pathway in LIN28B-Dependent Cancer Cells.International journal of molecular sciences · 2024Article
- Unveiling novel insights in acute myeloid leukemia through single-cell RNA sequencing.Frontiers in oncology · 2024Review
- Aberrant stem cell and developmental programs in pediatric leukemia.Frontiers in cell and developmental biology · 2024Review
- Review
- The LIN28B-let-7-PBK pathway is essential for group 3 medulloblastoma tumor growth and survival.Molecular oncology · 2023Article
- Structural Modifications and Novel Protein-Binding Sites in Pre-miR-675-Explaining Its Regulatory Mechanism in Carcinogenesis.Non-coding RNA · 2023Article
- BTYNB, an inhibitor of RNA binding protein IGF2BP1 reduces proliferation and induces differentiation of leukemic cancer cells.Saudi journal of biological sciences · 2023Article
- Inhibition of IGF2BP1 attenuates renal injury and inflammation by alleviating m6A modifications and E2F1/MIF pathway.International journal of biological sciences · 2023Article
- RNA binding proteins in MLL-rearranged leukemia.Experimental hematology & oncology · 2022Review
- The role of insulin-like growth factor 2 mRNA binding proteins in female reproductive pathophysiology.Reproductive biology and endocrinology : RB&E · 2022Review
- m6A modification: recent advances, anticancer targeted drug discovery and beyond.Molecular cancer · 2022Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCurrent conventional chemotherapy for acute myeloid leukemia (AML) can achieve remission in over 70% of patients, but a majority of them will relapse within 5 years despite continued treatment. The relapse is postulated to be due to leukemia stem cells (LSCs), which are different from normal hematopoietic stem cells (HSCs). LIN28B is microRNA regulator and stem cell reprogramming factor. Overexpression of LIN28B has been associated with advance human malignancies and cancer stem cells (CSCs), including AML. However, the molecular mechanism by which LIN28B contributes to the development of AML remains largely elusive.
methodsWe modulated LIN28B expression in AML and non-leukemic cells and investigated functional consequences in cell proliferation, cell cycle, and colony-forming assays. We performed a microarray-based analysis for LIN28B-silencing cells and interrogated gene expression data with different bioinformatic tools. AML mouse xenograft model was used to examine the in vivo function of LIN28B.
resultsWe demonstrated that targeting LIN28B in AML cells resulted in cell cycle arrest, inhibition of cell proliferation and colony formation, which was induced by de-repression of let-7a miRNA. On the other hand, overexpression of LIN28B promoted cell proliferation. Data point to a mechanism where that inhibition of LIN28B induces metabolic changes in AML cells. IGF2BP1 was confirmed to be a novel downstream target of LIN28B via let-7 miRNA in AML. Notably, ectopic expression of LIN28B increased tumorigenicity, while silencing LIN28B led to slow tumor growth in vivo.
conclusionsIn sum, these results uncover a novel mechanism of an important regulatory signaling, LIN28B/let-7/IGF2BP1, in leukemogenesis and provide a rationale to target this pathway as effective therapeutic strategy.
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