ArticleBioengineered2022
Dihydroartemisinin represses oral squamous cell carcinoma progression through downregulating mitochondrial calcium uniporter.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 12 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
12 citing papers in PubMed, 20 citations in OpenAlex.
- Mitochondrial CaJournal of cellular physiology · 2025Review
- MCU complex: Exploring emerging targets and mechanisms of mitochondrial physiology and pathology.Journal of advanced research · 2025Review
- Synthetic Vesicle-Based Drug Delivery Systems for Oral Disease Therapy: Current Applications and Future Directions.Journal of functional biomaterials · 2025Review
- Artemisinin derivatives maintain fibroblast normalization by acting on tumor-stroma interactions in oral tongue squamous cell carcinoma.American journal of cancer research · 2025Article
- Anti-Cancer Potential of Phytochemicals: The Regulation of the Epithelial-Mesenchymal Transition.Molecules (Basel, Switzerland) · 2023Review
- Critical roles of adherens junctions in diseases of the oral mucosa.Tissue barriers · 2023Article
- The role of novel programmed cell death in head and neck squamous cell carcinoma: from mechanisms to potential therapies.Frontiers in pharmacology · 2023Review
- The role of nanotherapy in head and neck squamous cell carcinoma by targeting tumor microenvironment.Frontiers in immunology · 2023Review
- Repurposing Dihydroartemisinin to Combat Oral Squamous Cell Carcinoma, Associated with Mitochondrial Dysfunction and Oxidative Stress.Oxidative medicine and cellular longevity · 2023Article
- Calcium signaling in neurodevelopment and pathophysiology of autism spectrum disorders.Molecular biology reports · 2022Review
- The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells.International journal of molecular sciences · 2022Review
- Article
Corrections and comments
- Retracted
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulation of mitochondrial calcium uniporter (MCU) exerts a carcinogenic effect in several cancers. Nevertheless, the roles of MCU in oral squamous cell carcinoma (OSCC) remain elusive. It has been reported that dihydroartemisinin (DHA) may suppress the progression of OSCC but its associated mechanisms have not been investigated. The purpose of our research was to observe the biological function of MCU on OSCC and its regulatory relationship with DHA. MCU, MICU1, MICU2, N-cadherin, TGF-β and vimentin expression was detected in OSCC and peritumoral tissues by immunohistochemistry and Western blot. Following DHA treatment, the expression of the aforementioned proteins was detected in CAL-27 cells transfected with shMCU or pcDNA3.1-MCU by Western blot or immunofluorescence. Furthermore, clone formation, mitochondrial membrane potential (MMP), wound healing and transwell assays were presented in CAL-27 cells treated with DHA, shMCU or pcDNA3.1-MCU. Our results showed that the members of MCU complex (MCU, MICU1 and MICU2) were overexpressed in OSCC than peritumoral tissues. Furthermore, TGF-β and epithelial to mesenchymal transition (EMT) proteins (N-cadherin and vimentin) exhibited higher expression in OSCC. DHA treatment significantly lowered the expression of MCU in CAL-27 cells. MCU overexpression reversed the inhibitory effects of DHA on MICU1, MICU2, N-cadherin, TGF-β and vimentin. MCU knockdown or DHA suppressed proliferation, MMP and migration of CAL-27 cells. DHA treatment could reverse the effects of MCU overexpression. Collectively, our study demonstrated that MCU was an oncogene of OSCC and DHA exerted a suppressive role on proliferation and migration of OSCC cells by suppressing MCU expression.
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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.