ReviewTrends in molecular medicine2020
The Mitochondrion as an Emerging Therapeutic Target in Cancer.
Review in Trends in molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
113 citing papers in PubMed.
- PINK1 promotes the progression of lung squamous cell carcinoma through the FAK/AKT/RhoA/vinculin pathway.Oncology reports · 2026Article
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- Tumoricidal efficacy of DZ-1 dye conjugated to dihydroartemisinin in patient-derived colorectal liver metastasis tumoroids.Molecular therapy. Oncology · 2026Article
- In vitro cytotoxic and apoptotic effects of chitosan-coated gold nanoparticles on HT-29 human colorectal adenocarcinoma cells.BMC gastroenterology · 2026Article
- Review
- Review
- MRPL42 Knockdown Suppresses the Malignant Functions of Hepatocellular Carcinoma by Regulating Oxidative Phosphorylation.Current medical science · 2026Article
- NRIP1 co-activates nuclear translocated FOXO3 to upregulate TFAM expression and promote radioresistance in non-small cell lung cancer.Cell death discovery · 2026Article
- SHMT2 inhibition triggers mitochondrial apoptosis to suppress lung adenocarcinoma progression.Journal of translational medicine · 2026Article
- Integrated single-cell and transcriptomic analysis of CD8Translational cancer research · 2026Article
- Pharmacological Myristoylation Inhibition by Zelenirstat Disrupts Growth Signalling, Energy Metabolism, and Migration in Triple-Negative Breast Cancer Cells.Breast cancer (Dove Medical Press) · 2026Article
- Targeting Metabolism in Cancer Therapy: Inhibitors and Approaches.Cancer treatment and research · 2026Review
- Metabolic reprogramming in diffuse intrinsic pontine gliomas (DIPG): dual inhibition of mitochondrial oxidative phosphorylation and lactate metabolism to enhance anti-tumor and radiosensitizing effects in DIPG cells.Cancer & metabolism · 2025Article
- Mitochondrial ribosomal protein L12 mediates metabolic reorganization in clear cell renal cell carcinoma by regulating mitochondrial biosynthesis.Cell communication and signaling : CCS · 2025Article
- The Critical Role of Enhanced OXPHOS and Mitochondrial Hyperpolarization in Simulated Microgravity-Induced Oocyte Maturation Arrest.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The role of mitochondria-related genes in hepatocellular carcinoma prognosis: construction of prognostic models based on machine learning.Discover oncology · 2025Article
- Metabolic pathways in deep vein thrombosis: a new frontier for therapeutic intervention.Blood · 2025Review
- Article
- Screening of patient-derived organoids identifies mitophagy as a cell-intrinsic vulnerability in colorectal cancer during statin treatment.Cell reports. Medicine · 2025Article
- Comprehensive analysis of mitochondrial-related gene signature for prognosis, tumor immune microenvironment evaluation, and candidate drug development in colon cancer.Scientific reports · 2025Article
53 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Mitochondria have emerged as important pharmacological targets because of their key role in cellular proliferation and death. In tumor tissues, mitochondria can switch metabolic phenotypes to meet the challenges of high energy demand and macromolecular synthesis. Furthermore, mitochondria can engage in crosstalk with the tumor microenvironment, and signals from cancer-associated fibroblasts can impinge on mitochondria. Cancer cells can also acquire a hybrid phenotype in which both glycolysis and oxidative phosphorylation (OXPHOS) can be utilized. This hybrid phenotype can facilitate metabolic plasticity of cancer cells more specifically in metastasis and therapy-resistance. In light of the metabolic heterogeneity and plasticity of cancer cells that had until recently remained unappreciated, strategies targeting cancer metabolic dependency appear to be promising in the development of novel and effective cancer therapeutics.
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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.