ArticleOncotarget2016
Different BCR/Abl protein suppression patterns as a converging trait of chronic myeloid leukemia cell adaptation to energy restriction.
Article in Oncotarget, 2016. 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, 22 citations in OpenAlex.
- Lactate-mediated activation of GPR81 regulates BCR/Abl protein expression in chronic myeloid leukemia cells selected under low oxygen tension.The Journal of pathology · 2025Article
- The MEK5/ERK5 pathway promotes the activation of the Hedgehog/GLI signaling in melanoma cells.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- BCR::ABL1 expression in chronic myeloid leukemia cells in low oxygen is regulated by glutamine via CD36-mediated fatty acid uptake.Cancer cell international · 2025Article
- Liquid Crystalline Networks Hamper the Malignancy of Cancer Cells.Advanced healthcare materials · 2025Article
- A New Algorithm Integrating Molecular Response, Toxicity, and Plasma Level Measures for Ponatinib Dose Choice in Patients Affected by Chronic Myeloid Leukemia.Pharmaceutics · 2024Article
- Lactate Maintains BCR/Abl Expression and Signaling in Chronic Myeloid Leukemia Cells Under Nutrient Restriction.Oncology research · 2022Article
- Article
- Identification of an individualized autophagy prognostic index in clear cell renal cell carcinoma patients.Translational cancer research · 2020Article
- Construction of a prognostic model based on nine immune-related genes and identification of small molecule drugs for hepatocellular carcinoma (HCC).American journal of translational research · 2020Article
- Identification and validation of an individualized autophagy-clinical prognostic index in bladder cancer patients.OncoTargets and therapy · 2019Article
- Sensitivity to imatinib of KCL22 chronic myeloid leukemia cell survival/growth and stem cell potential under glucose shortage.Data in brief · 2018Article
- Targeting chronic myeloid leukemia stem cells with the hypoxia-inducible factor inhibitor acriflavine.Blood · 2017Article
- The Leukemic Stem Cell Niche: Adaptation to "Hypoxia" versus Oncogene Addiction.Stem cells international · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BCR/Abl protein drives the onset and progression of Chronic Myeloid Leukemia (CML). We previously showed that BCR/Abl protein is suppressed in low oxygen, where viable cells retain stem cell potential. This study addressed the regulation of BCR/Abl protein expression under oxygen or glucose shortage, characteristic of the in vivo environment where cells resistant to tyrosine kinase inhibitors (TKi) persist. We investigated, at transcriptional, translational and post-translational level, the mechanisms involved in BCR/Abl suppression in K562 and KCL22 CML cells. BCR/abl mRNA steady-state analysis and ChIP-qPCR on BCR promoter revealed that BCR/abl transcriptional activity is reduced in K562 cells under oxygen shortage. The SUnSET assay showed an overall reduction of protein synthesis under oxygen/glucose shortage in both cell lines. However, only low oxygen decreased polysome-associated BCR/abl mRNA significantly in KCL22 cells, suggesting a decreased BCR/Abl translation. The proteasome inhibitor MG132 or the pan-caspase inhibitor z-VAD-fmk extended BCR/Abl expression under oxygen/glucose shortage in K562 cells. Glucose shortage induced autophagy-dependent BCR/Abl protein degradation in KCL22 cells. Overall, our results showed that energy restriction induces different cell-specific BCR/Abl protein suppression patterns, which represent a converging route to TKi-resistance of CML cells. Thus, the interference with BCR/Abl expression in environment-adapted CML cells may become a useful implement to current therapy.
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