ArticleAmerican journal of translational research2020
The Lyn-SIRT1 signaling pathway is involved in imatinib resistance in chronic myeloid leukaemia.
Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Transcriptome profiling and metabolic pathway analysis towards reliable biomarker discovery in early-stage lung cancer.Journal of applied genetics · 2025Article
- The Role of SIRT1 in Leukemia.Current treatment options in oncology · 2024Review
- Role of SIRT1 in Chemoresistant Leukemia.International journal of molecular sciences · 2023Review
- The Underappreciated Role of Epithelial Mesenchymal Transition in Chronic Obstructive Pulmonary Disease and Its Strong Link to Lung Cancer.Biomolecules · 2021Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundImatinib resistance is commonly associated with the activation of BCR-ABL signaling in chronic myeloid leukaemia (CML). The activation of Lyn can result in imatinib resistance by regulating the formation of BCR-ABL protein complexes. SIRT1 is a novel survival pathway activated by BCR-ABL expression in haematopoietic progenitor cells. This study aimed to investigate whether the signaling pathway of Lyn/BCR-ABL/SIRT1 could mediate imatinib resistance in CML.
methodsThe MTT assay was used to detect cell viability. Apoptosis was measured by a flow cytometry assay. Protein expression was detected by Western blotting. Knockdown CML cells were constructed by shRNA interference. The CML mouse model was used to investigate the role of SIRT1 in CML
resultsLyn was overexpressed in K562R cells. BCR-ABL phosphorylation and activation were promoted by Lyn. Imatinib suppressed BCR-ABL phosphorylation in both K562 and K562R cells. BCR-ABL positively regulated SIRT1 and Foxo1 but negatively regulated acetylated Foxo1 (Ac-Foxo1) and p53 expression. Pharmacological inhibition of SIRT1 or knockdown of SIRT1 increased apoptosis and reduced growth
conclusionWe proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.
Indexed as
Identifiers
32655803PMC7344074W3043633672What OpenQuestion holds
Registered trials
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