ReviewOncogene2014
Mitochondrial matrix proteases as novel therapeutic targets in malignancy.
Review in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 83 citations in OpenAlex.
- Structural Analysis of Human LonP1 Protease Bound with the Native Substrate.Life (Basel, Switzerland) · 2026Article
- Molecular mechanisms of mitochondrial AAA+ proteases.The Journal of biological chemistry · 2026Review
- Mitochondria as key targets underlying hypomagnetic field-induced biological effects.iScience · 2026Review
- Mipep deficiency in adipocytes impairs mitochondrial protein maturation and leads to systemic inflammation and metabolic dysfunctions.Scientific reports · 2025Article
- Mechanism and Therapeutic Progress of One-Carbon Metabolic Key Enzyme: Serine Hydroxymethyltransferase 2 in Cancer.Clinical Medicine Insights. Oncology · 2025Review
- The mitochondrial protease ClpP is a druggable target that controls VSMC phenotype by a SIRT1-dependent mechanism.Redox biology · 2024Article
- ONC201 Suppresses Neuroblastoma Growth by Interrupting Mitochondrial Function and Reactivating Nuclear ATRX Expression While Decreasing MYCN.International journal of molecular sciences · 2023Article
- mtUPR Modulation as a Therapeutic Target for Primary and Secondary Mitochondrial Diseases.International journal of molecular sciences · 2023Review
- Mitochondrial oxidative stress in the tumor microenvironment and cancer immunoescape: foe or friend?Journal of biomedical science · 2022Review
- Insight into the mitochondrial unfolded protein response and cancer: opportunities and challenges.Cell & bioscience · 2022Review
- GBAS Regulates the Proliferation and Metastasis of Ovarian Cancer Cells by Combining with eEF1A1.The oncologist · 2022Article
- The Role of Mitochondrial Quality Control in Anthracycline-Induced Cardiotoxicity: From Bench to Bedside.Oxidative medicine and cellular longevity · 2022Review
- Mitochondrial dysfunction, UPRCell & bioscience · 2021Review
- Caseinolytic protease P (CLPP) activated by ONC201 inhibits proliferation and promotes apoptosis in human epithelial ovarian cancer cells by inducing mitochondrial dysfunction.Annals of translational medicine · 2021Article
- Mitochondrial Lon protease is a gatekeeper for proteins newly imported into the matrix.Communications biology · 2021Article
- Suppression of Pyruvate Dehydrogenase Kinase by Dichloroacetate in Cancer and Skeletal Muscle Cells Is Isoform Specific and Partially Independent of HIF-1α.International journal of molecular sciences · 2021Article
- Article
- Mitochondrial ATP-Dependent Proteases-Biological Function and Potential Anti-Cancer Targets.Cancers · 2021Review
- LONP1 and ClpP cooperatively regulate mitochondrial proteostasis for cancer cell survival.Oncogenesis · 2021Article
- The Mitochondrial Protease LonP1 Promotes Proteasome Inhibitor Resistance in Multiple Myeloma.Cancers · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although mitochondrial function is often altered in cancer, it remains essential for tumor viability. Tight control of protein homeostasis is required for the maintenance of mitochondrial function, and the mitochondrial matrix houses several coordinated protein quality control systems. These include three evolutionarily conserved proteases of the AAA+ superfamily-the Lon, ClpXP and m-AAA proteases. In humans, these proteases are proposed to degrade, process and chaperone the assembly of mitochondrial proteins in the matrix and inner membrane involved in oxidative phosphorylation, mitochondrial protein synthesis, mitochondrial network dynamics and nucleoid function. In addition, these proteases are upregulated by a variety of mitochondrial stressors, including oxidative stress, unfolded protein stress and imbalances in respiratory complex assembly. Given that tumor cells must survive and proliferate under dynamic cellular stress conditions, dysregulation of mitochondrial protein quality control systems may provide a selective advantage. The association of mitochondrial matrix AAA+ proteases with cancer and their potential for therapeutic modulation therefore warrant further consideration. Although our current knowledge of the endogenous human substrates of these proteases is limited, we highlight functional insights gained from cultured human cells, protease-deficient mouse models and other eukaryotic model organisms. We also review the consequences of disrupting mitochondrial matrix AAA+ proteases through genetic and pharmacological approaches, along with implications of these studies on the potential of these proteases as anticancer therapeutic targets.
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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.