ArticleJournal of experimental & clinical cancer research : CR2017
Inhibition of autophagy enhances the selective anti-cancer activity of tigecycline to overcome drug resistance in the treatment of chronic myeloid leukemia.
Article in Journal of experimental & clinical cancer research : CR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 53 citations in OpenAlex.
- Off-target anti-leukemic effects of antibiotics: mechanisms and therapeutic insights.Cancer chemotherapy and pharmacology · 2026Review
- A selenium-containing selective estrogen receptor modulator to overcome drug resistance of chronic myeloid leukemia.Apoptosis : an international journal on programmed cell death · 2026Article
- SH3BP5-driven metabolic-immune crosstalk in DLBCL: a prognostic biomarker and therapeutic target for reshaping immunosuppressive microenvironment.Journal of translational medicine · 2025Article
- Autophagy and Cancer: Insights into Molecular Mechanisms and Therapeutic Approaches for Chronic Myeloid Leukemia.Biomolecules · 2025Review
- Circular RNAs and Cancers.Advances in experimental medicine and biology · 2025Review
- Third-Generation Tetracyclines: Current Knowledge and Therapeutic Potential.Biomolecules · 2024Review
- Drug Repurposing of Selected Antibiotics: An Emerging Approach in Cancer Drug Discovery.ACS omega · 2024Review
- Tigecycline Opposes Bortezomib Effect on Myeloma Cells Decreasing Mitochondrial Reactive Oxygen Species Production.International journal of molecular sciences · 2024Article
- CRIP1 involves the pathogenesis of multiple myeloma via dual-regulation of proteasome and autophagy.EBioMedicine · 2024Article
- Repurposed Drugs in Gastric Cancer.Molecules (Basel, Switzerland) · 2022Review
- Mitochondrial adaptation in cancer drug resistance: prevalence, mechanisms, and management.Journal of hematology & oncology · 2022Review
- Autophagy activation mediates resistance to FLT3 inhibitors in acute myeloid leukemia with FLT3-ITD mutation.Journal of translational medicine · 2022Article
- Advances in the Study of circRNAs in Hematological Malignancies.Frontiers in oncology · 2022Review
- Resistance to Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia-From Molecular Mechanisms to Clinical Relevance.Cancers · 2021Review
- Review
- PINK1/Parkin-mediated mitophagy inhibits warangalone-induced mitochondrial apoptosis in breast cancer cells.Aging · 2021Article
- Pancreatic Cancer and Therapy: Role and Regulation of Cancer Stem Cells.International journal of molecular sciences · 2021Review
- Targeting Abnormal Hematopoietic Stem Cells in Chronic Myeloid Leukemia and Philadelphia Chromosome-Negative Classical Myeloproliferative Neoplasms.International journal of molecular sciences · 2021Review
- Medicinal Chemistry Targeting Mitochondria: From New Vehicles and Pharmacophore Groups to Old Drugs with Mitochondrial Activity.International journal of molecular sciences · 2020Review
- Targeting the Mitochondrial Metabolic Network: A Promising Strategy in Cancer Treatment.International journal of molecular sciences · 2020Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDrug resistance and disease progression are still the major obstacles in the treatment of chronic myeloid leukemia (CML). Increasing researches have demonstrated that autophagy becomes activated when cancer cells are subjected to chemotherapy, which is involved in the development of drug resistance. Therefore, combining chemotherapy with inhibition of autophagy serves as a new strategy in cancer treatment. Tigecycline is an antibiotic that has received attention as an anti-cancer agent due to its inhibitory effect on mitochondrial translation. However, whether combination of tigecycline with inhibition of autophagy could overcome drug resistance in CML remains unclear.
methodsWe analyzed the biological and metabolic effect of tigecycline on CML primary cells and cell lines to investigate whether tigecycline could regulate autophagy in CML cells and whether coupling autophagy inhibition with treatment using tigecycline could affect the viabilities of drug-sensitive and drug-resistant CML cells.
resultsTigecycline inhibited the viabilities of CML primary cells and cell lines, including those that were drug-resistant. This occurred via the inhibition of mitochondrial biogenesis and the perturbation of cell metabolism, which resulted in apoptosis. Moreover, tigecycline induced autophagy by downregulating the PI3K-AKT-mTOR pathway. Additionally, combining tigecycline use with autophagy inhibition further promoted the anti-leukemic activity of tigecycline. We also observed that the anti-leukemic effect of tigecycline is selective. This is because the drug targeted leukemic cells but not normal cells, which is because of the differences in the mitochondrial biogenesis and metabolic characterization between the two cell types.
conclusionsCombining tigecycline use with autophagy inhibition is a promising approach for overcoming drug resistance in CML treatment.
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