ArticleAutophagy2016
ATG7 regulates energy metabolism, differentiation and survival of Philadelphia-chromosome-positive cells.
Article in Autophagy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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
68 citing papers in PubMed, 109 citations in OpenAlex.
- Myeloid differentiation-associated autophagy drives venetoclax resistance in AML.Research square · 2026Article
- Targeting Mitochondrial Vulnerabilities in Chronic Myeloid Leukemia: From Pathobiology to Novel Therapeutic Opportunities.Cancers · 2026Review
- Hsp70-Bim interaction mediated mitophagy as a potential therapeutic target for CML stem cells.Stem cell reports · 2026Article
- Targeting Lysosomes for Enhanced Anti-Cancer Therapeutics and Immune Response.International journal of biological sciences · 2026Review
- ATG7-driven mitophagy in BMSC@CS hydrogel reprograms metabolism to boost bone regeneration.Materials today. Bio · 2025Article
- A novel regulatory circuit of ATG4B and SESN3 promotes T cell leukemogenesis.Journal of experimental & clinical cancer research : CR · 2025Article
- The dual role of autophagy in cancer stem cells: implications for tumor progression and therapy resistance.Journal of translational medicine · 2025Review
- Autophagy Related 5 Promotes Mitochondrial Fission and Inflammation via HSP90-HIF-1α-Mediated Glycolysis in Kidney Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- PTBP2 promotes cell survival and autophagy in chronic myeloid leukemia by stabilizing BNIP3.Cell death & disease · 2025Article
- The role of autophagy in cancer: from molecular mechanism to therapeutic window.Frontiers in immunology · 2025Review
- Current Understanding of the Role of Autophagy in the Treatment of Myeloid Leukemia.International journal of molecular sciences · 2024Review
- Oxidative Stress and Chronic Myeloid Leukemia: A Balance between ROS-Mediated Pro- and Anti-Apoptotic Effects of Tyrosine Kinase Inhibitors.Antioxidants (Basel, Switzerland) · 2024Review
- Crosstalk between metabolism and cell death in tumorigenesis.Molecular cancer · 2024Review
- ATG7(2) Interacts With Metabolic Proteins and Regulates Central Energy Metabolism.Traffic (Copenhagen, Denmark) · 2024Article
- mTOR inhibition by AZD2014 alleviates BCR::ABL1 independent imatinib resistance through enhancing autophagy in CML resistant cells.American journal of cancer research · 2024Article
- Review
- Tumor microenvironment-induced tumor cell plasticity: relationship with hypoxic stress and impact on tumor resistance.Frontiers in oncology · 2023Review
- Elucidation of the Role of FAM210B in Mitochondrial Metabolism and Erythropoiesis.Molecular and cellular biology · 2022Article
- Article
- A Mitophagy-Related Gene Signature for Subtype Identification and Prognosis Prediction of Hepatocellular Carcinoma.International journal of molecular sciences · 2022Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 8 institutions in 2 countries.
Funding
Abstract
A major drawback of tyrosine kinase inhibitor (TKI) treatment in chronic myeloid leukemia (CML) is that primitive CML cells are able to survive TKI-mediated BCR-ABL inhibition, leading to disease persistence in patients. Investigation of strategies aiming to inhibit alternative survival pathways in CML is therefore critical. We have previously shown that a nonspecific pharmacological inhibition of autophagy potentiates TKI-induced death in Philadelphia chromosome-positive cells. Here we provide further understanding of how specific and pharmacological autophagy inhibition affects nonmitochondrial and mitochondrial energy metabolism and reactive oxygen species (ROS)-mediated differentiation of CML cells and highlight ATG7 (a critical component of the LC3 conjugation system) as a potential specific therapeutic target. By combining extra- and intracellular steady state metabolite measurements by liquid chromatography-mass spectrometry with metabolic flux assays using labeled glucose and functional assays, we demonstrate that knockdown of ATG7 results in decreased glycolysis and increased flux of labeled carbons through the mitochondrial tricarboxylic acid cycle. This leads to increased oxidative phosphorylation and mitochondrial ROS accumulation. Furthermore, following ROS accumulation, CML cells, including primary CML CD34(+) progenitor cells, differentiate toward the erythroid lineage. Finally, ATG7 knockdown sensitizes CML progenitor cells to TKI-induced death, without affecting survival of normal cells, suggesting that specific inhibitors of ATG7 in combination with TKI would provide a novel therapeutic approach for CML patients exhibiting persistent disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.