ArticleAmerican journal of cancer research2015
Effects of topoisomerase inhibitors that induce DNA damage response on glucose metabolism and PI3K/Akt/mTOR signaling in multiple myeloma cells.
Article in American journal of cancer research, 2015. 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, 40 citations in OpenAlex.
- Integrin-linked kinase (ILK) in hematologic malignancies: Bridging molecular mechanisms to therapeutic innovation.BioImpacts : BI · 2026Review
- Mesenchymal stromal cells in bone marrow niche of patients with multiple myeloma: a double-edged sword.Cancer cell international · 2025Review
- Nestin in multiple myeloma: emerging insights into a potential therapeutic target.Frontiers in oncology · 2025Review
- Targeting the DNA damage response in hematological malignancies.Frontiers in oncology · 2024Review
- Shutting off the fuel supply to target metabolic vulnerabilities in multiple myeloma.Frontiers in oncology · 2023Review
- Metformin Attenuates UVA-Induced Skin Photoaging by Suppressing Mitophagy and the PI3K/AKT/mTOR Pathway.International journal of molecular sciences · 2022Article
- Emerging Glycation-Based Therapeutics-Glyoxalase 1 Inducers and Glyoxalase 1 Inhibitors.International journal of molecular sciences · 2022Review
- Metabolic features of myeloma cells in the context of bone microenvironment: Implication for the pathophysiology and clinic of myeloma bone disease.Frontiers in oncology · 2022Review
- Contribution of the Tumor Microenvironment to Metabolic Changes Triggering Resistance of Multiple Myeloma to Proteasome Inhibitors.Frontiers in oncology · 2022Review
- The related miRNAs involved in doxorubicin resistance or sensitivity of various cancers: an update.Cancer chemotherapy and pharmacology · 2021Review
- Metabolic Disorders in Multiple Myeloma.International journal of molecular sciences · 2021Review
- A pilot study of 3D tissue-engineered bone marrow culture as a tool to predict patient response to therapy in multiple myeloma.Scientific reports · 2021Observational
- Studies of Glyoxalase 1-Linked Multidrug Resistance Reveal Glycolysis-Derived Reactive Metabolite, Methylglyoxal, Is a Common Contributor in Cancer Chemotherapy Targeting the Spliceosome.Frontiers in oncology · 2021Article
- The inhibition of MARK2 suppresses cisplatin resistance of osteosarcoma stem cells by regulating DNA damage and repair.Journal of bone oncology · 2020Article
- Role of HSP27 in the multidrug sensitivity and resistance of colon cancer cells.Oncology letters · 2020Article
- Review
- Vulnerabilities of the SARS-CoV-2 Virus to Proteotoxicity-Opportunity for Repurposed Chemotherapy of COVID-19 Infection.Frontiers in pharmacology · 2020Article
- TOP2A Promotes Lung Adenocarcinoma Cells' Malignant Progression and Predicts Poor Prognosis in Lung Adenocarcinoma.Journal of Cancer · 2020Article
- Metabolic Reprogramming Induces Immune Cell Dysfunction in the Tumor Microenvironment of Multiple Myeloma.Frontiers in oncology · 2020Review
- Magnetic Resonance Imaging Is More Sensitive Than PET for Detecting Treatment-Induced Cell Death-Dependent Changes in Glycolysis.Cancer research · 2019Article
Corrections and comments
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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
Hallmarks of cancer cells comprise altered glucose metabolism (aerobic glycolysis) and differences in DNA damage response (DDR). Glucose transporters (GLUT), glycolytic enzymes such as hexokinase (HK) and metabolic pathways (e.g. PI3K/Akt/mTor) have been shown to be upregulated in multiple myeloma and other cancer cell lines. Here we have investigated the effects of clinically used inhibitors of topoisomerases, of DDR and of the PI3K/Akt/mTor pathway on glucose metabolism and on cell survival in multiple myeloma cells. The effects of DNA damaging topoisomerase inhibitors (doxorubicin, etoposide, topotecan), non-DNA damaging agents (bortezomib, vincristine) as well as of molecular inhibitors of DNA damage related kinases PIKKs (KU55933 [ATM], NU7026 [DNA-PKCs]) and PI3K/Akt/mTor signaling (BEZ235 [PI3K/mTor], MK-2206 [Akt]) were analyzed 24 hours after treatment of OPM-2 multiple myeloma cells. For this purpose we monitored [18F]-FDG uptake, cell viability using an ATP assay and expression of GLUT-1, hexokinase II (HKII), cleaved caspase-3 and cleaved PARP via Western-blotting. All topoisomerase inhibitors used could upregulate expression of GLUT-1 and HKII in OPM-2 cells, resulting in elevated [18F]-FDG uptake and promotion of cell survival. In contrast, bortezomib and vincristine induced a decline in [18F]-FDG uptake combined with early induction of apoptosis. Combination treatment with topoisomerase inhibitors and molecular inhibitors of PIKK and PI3K could reverse elevated [18F]-FDG uptake, as observed after application of topoisomerase inhibitors only, and aggravate induction of apoptosis. Thus, elevated glucose consumption in OPM-2 cells can be reversed by targeting both DDR and PI3K/Akt/mTOR signaling, thus providing a promising strategy in the treatment of cancer.
Indexed as
Identifiers
26175935PMC4497433W2398262997What OpenQuestion holds
Registered trials
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