ArticleScientific reports2022
ACSL1 promotes imatinib-induced chronic myeloid leukemia cell senescence by regulating SIRT1/p53/p21 pathway.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Exploiting cellular senescence in hematologic malignancies.Translational oncology · 2026Review
- Exploring the Therapeutic Effect ofNutrients · 2026Article
- Loss of ACSL1 fuels ferroptosis resistance in clear cell renal carcinoma.Cancer biology & therapy · 2025Article
- Long-chain acyl-CoA synthetases: biological functions, diseases and therapeutic targets.Molecular biomedicine · 2025Review
- Reprogramming of fatty acid metabolism in thyroid cancer: Potential targets and mechanisms.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025Article
- Enhanced induction of apoptosis in chronic myeloid leukemia cells through synergistic effect of telomerase inhibitor MST-312 and imatinib.Molecular biology reports · 2024Article
- Huaier inhibits autophagy and promotes apoptosis in T-cell acute lymphoblastic leukemia by down-regulating SIRT1.Heliyon · 2024Article
- Platelet microparticles influence gene expression and modulate biological activities of chronic myeloid leukemia cells (K562).Molecular biology reports · 2024Article
- Paeonol Attenuates Atherosclerosis by Inhibiting Vascular Smooth Muscle Cells Senescence via SIRT1/P53/TRF2 Signaling Pathway.Molecules (Basel, Switzerland) · 2024Article
- 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
- Identification of hub genes and pathways associated with cellular senescence in diabetic foot ulcers via comprehensive transcriptome analysis.Journal of cellular and molecular medicine · 2024Article
- Ginsenosides on stem cells fate specification-a novel perspective.Frontiers in cell and developmental biology · 2023Review
- Loss of G0/G1 switch gene 2 (G0S2) promotes disease progression and drug resistance in chronic myeloid leukaemia (CML) by disrupting glycerophospholipid metabolism.Clinical and translational medicine · 2022Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although tyrosine kinase inhibitors (TKIs) improve the prognosis of chronic myeloid leukemia (CML) patients, resistance to TKIs and residual leukemia stem cells (LSCs) inevitably become the bottleneck of cure. Therefore, we need to explore novel treatment strategies based on conventional treatment strategies. Our previous study found that CML cell senescence may be one of the main factors to achieve clinical cure of CML. Studies have shown that lipid metabolism plays a key role in cellular senescence. Here, we found that long-chain acyl-CoA synthetase 1 (ACSL1) was significantly up-regulated in senescent CML cells. Furthermore, we demonstrated that overexpression of ACSL1 induces senescence and inhibits cell growth in K562 cells by altering cell cycle progression, and enhances the proliferation-inhibiting effect of imatinib. Overexpression of ACSL1 enhances imatinib-induced tumorigenic decline in K562 cells in vivo. Knockdown of ACSL1 reverses imatinib-induced senescence in K562 cells. Mechanistically, overexpression of ACSL1 induced senescence in K562 cells via the SIRT1/p53/p21 axis. Collectively, our study showed that ACSL1 promotes imatinib-induced K562 cells senescence and tumor growth by regulating SIRT1/p53/p21 pathway. The ACSL1/SIRT1/p53 signal axis is a novel mechanism of cell senescence in CML and a new potential target for eradication of CML LSCs.
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