ArticleJournal of hepatocellular carcinoma2022
Protodioscin Induces Mitochondrial Apoptosis of Human Hepatocellular Carcinoma Cells Through Eliciting ER Stress-Mediated IP3R Targeting Mfn1/Bak Expression.
Article in Journal of hepatocellular carcinoma, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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
16 citing papers in PubMed, 15 citations in OpenAlex.
- A tri-target in silico analysis of Testolift: a nutraceutical formulation targeting aromatase, myostatin, and prolyl hydroxylase-2 in testosterone regulation and muscle performance.Scientific reports · 2026Article
- Review
- Neuronal mitochondrial dynamics: roles in brain disorders and therapeutic potential.Acta pharmacologica Sinica · 2026Article
- Article
- Protodioscin enhances Methotrexate-induced senescence and senolytic activity in HepG2 liver cancer spheroids by modulating cell cycle regulators and the TGF-β/p-Smad2-4 signaling pathway.Scientific reports · 2025Article
- A comprehensive review on the role of plant-derived bioactive metabolites driving ROS-mediated apoptosis in cancer.Medical oncology (Northwood, London, England) · 2025Review
- Assessments of protodioscin's antinociceptive and antidiarrheal properties: in vivo and in silico investigations on macromolecule binding affinity and modulatory effects.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Targeting LC3B/MCL-1 expression by Protodioscin induces autophagy and apoptosis in human glioblastoma cellsInternational journal of medical sciences · 2025Article
- Shockwave-driven activation of endoplasmic reticulum stress in osteoblasts to enhance bone formation under osteoporotic conditions.Regenerative biomaterials · 2025Article
- A detailed review of pharmacology of MFN1 (mitofusion-1)-mediated mitochondrial dynamics: Implications for cellular health and diseases.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024Review
- The role of mitochondrial dynamics in disease.MedComm · 2023Review
- Recent advances in melittin-based nanoparticles for antitumor treatment: from mechanisms to targeted delivery strategies.Journal of nanobiotechnology · 2023Review
- Mitochondrial Dynamics in Neurodegenerative Diseases: Unraveling the Role of Fusion and Fission Processes.International journal of molecular sciences · 2023Review
- Oncogenic Proteomics Approaches for Translational Research and HIV-Associated Malignancy Mechanisms.Proteomes · 2023Review
- Article
- Blockage of Autophagy Increases Timosaponin AIII-Induced Apoptosis of Glioma Cells In Vitro and In Vivo.Cells · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Protodioscin (PD), a steroidal saponin, has a diverse pharmacological activity including neuroprotection, male fertility improvement, and cytotoxicity against various cancers cell lines of different origins. However, the effect of PD on hepatocellular carcinoma (HCC) is still unclear. Methods: Cell viability, colony formation and flow cytometry analysis for apoptosis profile, mitochondrial membrane potential endoplasmic reticulum (ER) expansion were employed to determine the effect of PD against HCC cells. Transient transfection of siRNA, immunofluorescent imaging and immunoprecipitation were used to elucidate the anti-cancer mechanism of PD. The in vivo toxicity and efficacy of PD were assessed by a xenograft mouse model. Results: PD induced apoptosis, loss of mitochondrial membrane potential and ER expansion in HCC cells. Either downregulation of Mfn1 or Bak reversed PD-induced apoptosis and loss of mitochondrial membrane potential. Further analysis revealed that Mfn1 and Bak will form a complex with IP3R to facilitate the transfer of Ca Conclusion: Our study sheds light on the understanding of the anti-HCC effects of PD and may open new aspects for the development of novel treatment for human hepatocellular carcinoma.
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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 Socratic graph.