ArticleOncotarget2016
Downregulation of HSP60 disrupts mitochondrial proteostasis to promote tumorigenesis and progression in clear cell renal cell carcinoma.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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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
37 citing papers in PubMed, 78 citations in OpenAlex.
- Regulatory networks of iron sulfur cluster biology in cancer mechanisms and therapeutic perspectives.iScience · 2026Review
- Oxalate induces proliferation and mitochondrial metabolism in select clear cell renal cell carcinoma cell lines.BMC cancer · 2026Article
- Review
- Protein modifications by advanced glycation end products (AGEs) in human clear cell renal cell carcinoma.Journal of translational medicine · 2025Article
- Therapeutic potential of melatonin-induced mitophagy in the pathogenesis of Alzheimer's disease.Inflammopharmacology · 2025Review
- Proteomic Analysis of Tear Films in Healthy Female and Male Dogs Using MALDI-TOF (Matrix Assisted Laser Desortion/Ionization Time-of-Flight) Mass Spectrometry.Animals : an open access journal from MDPI · 2025Article
- HSP60 controls mitochondrial ATP generation for optimal virus-specific IL-21-producing CD4 and cytotoxic CD8 memory T cell responses.Communications biology · 2024Article
- Review
- Prognosis value of heat-shock proteins in esophageal and esophagogastric cancer: A systematic review and meta-analysis.World journal of gastrointestinal oncology · 2024Article
- Intraneuronal β-amyloid impaired mitochondrial proteostasis through the impact on LONP1.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Knockdown of heat shock protein family D member 1 (HSPD1) promotes proliferation and migration of ovarian cancer cells via disrupting the stability of mitochondrial 3-oxoacyl-ACP synthase (OXSM).Journal of ovarian research · 2023Article
- The Journey of Mitochondrial Protein Import and the Roadmap to Follow.International journal of molecular sciences · 2023Review
- The mitochondrial unfolded protein response (UPRJournal of hematology & oncology · 2022Review
- Complex roles of nicotinamide N-methyltransferase in cancer progression.Cell death & disease · 2022Review
- Heat Shock Proteins and HSF1 in Cancer.Frontiers in oncology · 2022Review
- Review
- HSP60-knockdown suppresses proliferation in colorectal cancer cells via activating the adenine/AMPK/mTOR signaling pathway.Oncology letters · 2021Article
- Exploiting the HSP60/10 chaperonin system as a chemotherapeutic target for colorectal cancer.Bioorganic & medicinal chemistry · 2021Article
- Review
- Mitochondrial Dysfunction as a Driver of Cognitive Impairment in Alzheimer's Disease.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
In the present study, we demonstrate that HSP60 is unequivocally downregulated in clear cell renal cell carcinoma (ccRCC) tissues compared to pericarcinous tissues. Overexpression of HSP60 in ccRCC cancer cells suppresses cell growth. HSP60 knockdown increases cell growth and proliferation in both cell culture and nude mice xenografts, and drives cells to undergo epithelial to mesenchymal transition (EMT). Our results propose that HSP60 silencing disrupts the integrity of the respiratory complex I and triggers the excessive ROS production, which promotes tumor progression in the following aspects: (1) ROS activates the AMPK pathway that promotes acquisition of the Warburg phenotype in HSP60-KN cells; (2) ROS generated by HSP60 knockdown or by rotenone inhibition drives cells to undergo EMT; and (3) the high level of ROS may also fragment the Fe-S clusters that up regulates ADHFe1 expression and the 2-hydroxygluterate (2-HG) production leading to changes in DNA methylation. These results suggest that the high level of ROS is needed for tumorigenesis and progression in tumors with the low HSP60 expression and HSP60 is a potential diagnostic biomarker as well as a therapeutic target in ccRCC.
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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.