ReviewCells2019
Functional Compartmentalization of HSP60-Survivin Interaction between Mitochondria and Cytosol in Cancer Cells.
Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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.
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
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Prognostic and clinicopathological value of dbc1 expression in human cancers: a systematic review and meta-analysis.Frontiers in oncology · 2025Pooled it
- Hypoxia-ROS-HSP Triad Axis in Cancer: Mechanisms, Crosstalk, and Therapeutic Implications.Cells · 2026Review
- Melatonin ameliorates inflammation-induced mitochondrial dysfunction and cementoblastic differentiation in cells by regulating the METTL3/LINC01444/HSPD1 axis.Fundamental research · 2026Article
- GFAT2-mediated HSPD1 O-GlcNAcylation drives chemotherapy resistance in non-small cell lung cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- Pseudolaric acid B promotes lung cancer cells ferroptosis depending on JNK/ERK-mediated upregulation of survivin.Scientific reports · 2026Article
- Targeting the HSP60/p53 Axis with Extracellular Vesicle-Delivered siRNA Reprograms Glycolysis in Prostate Cancer.International journal of biological sciences · 2026Article
- Enhanced inhibitory effects of mianserin in combination with sorafenib on liver cancer growth through targeting the CCR9-AKT pathway.American journal of cancer research · 2025Article
- Identification and Clinical Validation of High HSP60 Expression Predicts Poor Prognosis in Patients with Ovarian Cancer.International journal of general medicine · 2025Article
- Potential of Natural Products in the Treatment of Glioma: Focus on Molecular Mechanisms.Cell biochemistry and biophysics · 2024Review
- Potential Anticancer Effects of Isoflavone Prunetin and Prunetin Glycoside on Apoptosis Mechanisms.International journal of molecular sciences · 2024Review
- LncRNAJournal of biomedical research · 2024Article
- Molecular Chaperonin HSP60: Current Understanding and Future Prospects.International journal of molecular sciences · 2024Review
- Review
- The Interplay between Heat Shock Proteins and Cancer Pathogenesis: A Novel Strategy for Cancer Therapeutics.Cancers · 2024Review
- HSPD1 Supports Osteosarcoma Progression through Stabilizing ATP5A1 and thus Activation of AKT/mTOR Signaling.International journal of biological sciences · 2024Article
- The proteomics analysis of extracellular vesicles revealed the possible function of heat shock protein 60 in Helicobacter pylori infection.Cancer cell international · 2023Article
- High expression of HSP60 and survivin predicts poor prognosis for oral squamous cell carcinoma patients.BMC oral health · 2023Article
- PRM-based quantitative proteomics analysis of altered HSP abundance in villi and decidua of patients with early missed abortion.Proteome science · 2023Article
- Clinicopathologic Significance of Heat Shock Protein 60 as a Survival Predictor in Colorectal Cancer.Cancers · 2023Article
- Exploring the Role of Hsp60 in Alzheimer's Disease and Type 2 Diabetes: Suggestion for Common Drug Targeting.International journal of molecular sciences · 2023Review
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
Heat shock protein 60 (HSP60) and survivin reside in both the cytosolic and mitochondrial compartments under physiological conditions. They can form HSP60-survivin complexes through protein-protein interactions. Their expression levels in cancer tissues are positively correlated and higher expression of either protein is associated with poor clinical prognosis. The subcellular location of HSP60-survivin complex in either the cytosol or mitochondria is cell type-dependent, while the biological significance of HSP60-survivin interaction remains elusive. Current knowledge indicates that the function of HSP60 partly rests on where HSP60-survivin interaction takes place. HSP60 has a pro-survival function when binding to survivin in the mitochondria through interacting with other factors such as CCAR2 and p53. In response to cell death signals, mitochondrial survivin functions through preventing procaspase activation. Degradation of cytosolic survivin leads to the loss of mitochondrial membrane potential and aberrant mitosis processes. On the other hand, HSP60 release from mitochondria to cytosol upon death stimuli might exert a pro-death function, either through stabilizing Bax, enhancing procaspase-3 activation, or increasing protein ubiquitination. Combining the knowledge of mitochondrial HSP60-survivin complex function, cytosolic survivin degradation effect, and pro-death function upon mitochondria release of HSP60, a hypothetical scenario for HSP60-survivin shuttling upon death stimuli is proposed.
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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.