ArticlePloS one2016
Minnelide/Triptolide Impairs Mitochondrial Function by Regulating SIRT3 in P53-Dependent Manner in Non-Small Cell Lung Cancer.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 34 citations in OpenAlex.
- TCM-Derived Small Molecules Targeting Metabolic Vulnerabilities in NSCLC: Ferroptosis-Centered Mechanisms and Emerging Cuproptosis- and Disulfidptosis-Related Vulnerabilities.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Antitumor natural products targeting mitochondrial NADH: ubiquinone oxidoreductase (complex I): a review.Frontiers in pharmacology · 2026Review
- The Interplay between Autophagy and Mitochondria in Cancer.International journal of molecular sciences · 2024Review
- A Bibliometric Analysis of Triptolide and the Recent Advances in Treating Non-Small Cell Lung Cancer.Frontiers in pharmacology · 2022Review
- Deacetylation of Transcription Factors in Carcinogenesis.International journal of molecular sciences · 2021Review
- Perspectives on the Clinical Development of NRF2-Targeting Drugs.Handbook of experimental pharmacology · 2021Review
- Minnelide, a prodrug, inhibits cervical cancer growth by blocking HPV-induced changes in p53 and pRb.American journal of cancer research · 2021Article
- Triptolide-induced apoptosis in non-small cell lung cancer via a novel miR204-5p/Caveolin-1/Akt-mediated pathway.Oncotarget · 2020Article
- Nitrite attenuates mitochondrial impairment and vascular permeability induced by ischemia-reperfusion injury in the lung.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- The Mitochondrion as an Emerging Therapeutic Target in Cancer.Trends in molecular medicine · 2020Review
- Triptolide attenuates lipopolysaccharide-induced inflammatory responses in human endothelial cells: involvement of NF-κB pathway.BMC complementary and alternative medicine · 2019Article
- The Roles of Plant-Derived Triptolide on Non-Small Cell Lung Cancer.Oncology research · 2019Review
- Naturally occurring anti-cancer compounds: shining from Chinese herbal medicine.Chinese medicine · 2019Review
- The Role of Herbal Bioactive Components in Mitochondria Function and Cancer Therapy.Evidence-based complementary and alternative medicine : eCAM · 2019Review
- Article
- Phytochemicals as modulators of M1-M2 macrophages in inflammation.Oncotarget · 2018Review
- Synergistic combination therapy of lung cancer using paclitaxel- and triptolide-coloaded lipid-polymer hybrid nanoparticles.Drug design, development and therapy · 2018Article
- Inducers of Senescence, Toxic Compounds, and Senolytics: The Multiple Faces of Nrf2-Activating Phytochemicals in Cancer Adjuvant Therapy.Mediators of inflammation · 2018Review
- Phylogeographic and phylogenetic analysis forEcology and evolution · 2017Article
- Pregnane X receptors regulate CYP2C8 and P-glycoprotein to impact on the resistance of NSCLC cells to Taxol.Cancer medicine · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Minnelide/Triptolide (TL) has recently emerged as a potent anticancer drug in non-small cell lung cancer (NSCLC). However, the precise mechanism of its action remains ambiguous. In this study, we elucidated the molecular basis for TL-induced cell death in context to p53 status. Cell death was attributed to dysfunction of mitochondrial bioenergetics in p53-deficient cells, which was characterized by decreased mitochondrial respiration, steady-state ATP level and membrane potential, but augmented reactive oxygen species (ROS). Increased ROS production resulted in oxidative stress in TL-treated cells. This was exhibited by elevated nuclear levels of a redox-sensitive transcriptional factor, NF-E2-related factor-2 (NRF2), along with diminished cellular glutathione (GSH) content. We further demonstrated that in the absence of p53, TL blunted the expression of mitochondrial SIRT3 triggering increased acetylation of NDUAF9 and succinate dehydrogenase, components of complexes I and II of the electron transport chain (ETC). TL-mediated hyperacetylation of complexes I and II proteins and these complexes displayed decreased enzymatic activities. We also provide the evidence that P53 regulate steady-state level of SIRT3 through Proteasome-Pathway. Finally, forced overexpression of Sirt3, but not deacetylase-deficient mutant of Sirt3 (H243Y), restored the deleterious effect of TL on p53-deficient cells by rescuing mitochondrial bioenergetics. On contrary, Sirt3 deficiency in the background of wild-type p53 triggered TL-induced mitochondrial impairment that echoed TL effect in p53-deficeint cells. These findings illustrate a novel mechanism by which TL exerts its potent effects on mitochondrial function and ultimately the viability of NSCLC tumor.
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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.