ArticleCancer management and research2020
Azoxystrobin Reduces Oral Carcinogenesis by Suppressing Mitochondrial Complex III Activity and Inducing Apoptosis.
Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Azoxystrobin induces mitochondrial dysfunction and mitochondrial pathway apoptosis by targeting the Prx1 Trp87 and Thr90 sites in oral leukoplakia.Frontiers in pharmacology · 2026Article
- Piperine Induces Apoptosis and Cell Cycle Arrest via Multiple Oxidative Stress Mechanisms and Regulation of PI3K/Akt and MAPK Signaling in Colorectal Cancer Cells.Antioxidants (Basel, Switzerland) · 2025Article
- Preparation of Azoxystrobin-Zinc Metal-Organic Framework/Biomass Charcoal Composite Materials and Application in the Prevention and Control of Gray Mold in Tomato.International journal of molecular sciences · 2023Article
- Review
- Azoxystrobin exposure impairs meiotic maturation by disturbing spindle formation in mouse oocytes.Frontiers in cell and developmental biology · 2022Article
- Azoxystrobin induces apoptosisFrontiers in pharmacology · 2022Article
- Azoxystrobin Impairs Neuronal Migration and Induces ROS Dependent Apoptosis in Cortical Neurons.International journal of molecular sciences · 2021Article
- Clinicopathological Significance of FOXO4 Expression and Correlation with Prx1 in Head and Neck Squamous Cell Carcinoma.Analytical cellular pathology (Amsterdam) · 2021Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe five-year survival rate of patients with oral cancer is approximately 50%; thus, alternative drugs with higher efficacy are urgently required. Azoxystrobin (AZOX), a natural, novel methoxyacrylate fungicide isolated from mushrooms, has a broad-spectrum, with highly efficient bactericidal effect. However, studies on AZOX have focused on antifungal effects. Here, we explore the potential cancer-preventive effects of AZOX and the underlying mechanisms. MATERIALS AND
methodsThe effects of AZOX on oral carcinogenesis induced by 4-nitroquinoline-1-oxide (4NQO) were investigated in C57BL/6 mice. Cell proliferation and apoptosis were examined by Ki67 immunohistochemistry and TUNEL staining, respectively. The main organ coefficients of each group were calculated to evaluate the biosafety of AZOX. CCK8 and flow cytometry were used to detect the effects of AZOX on cell viability and apoptosis in oral cancer cell line CAL27 and SCC15 cells in vitro. Cell cycle, mitochondrial complex III activity, intercellular reactive oxygen species (ROS) level, mitochondrial ROS level, and mitochondrial membrane potential (MMP) were detected by flow cytometry in AZOX-treated CAL27 cells.
resultsAZOX significantly inhibited the occurrence of 4NQO-induced tongue cancer and delayed the progression of tongue precancerous lesions in mice. High-dose AZOX obviously inhibited cell viability and induced apoptosis in epithelial dysplastic and oral squamous cell carcinoma (OSCC) lesions in mouse tongue mucosa. AZOX was confirmed to have high biosafety. Similarly, in vitro cell viability was suppressed, and apoptosis was induced in AZOX-treated CAL27 and SCC15 cells. AZOX induced cell cycle arrest at the S phase. AZOX inhibited mitochondrial complex III activity, increased intracellular and mitochondrial ROS levels, and decreased MMP in CAL27 cells.
conclusionAZOX inhibited the development of oral cancer through specific inhibition of the activity of mitochondrial complex III, which led to ROS accumulation, and MMP decrease, ultimately inducing apoptosis. AZOX may be a novel agent for the prevention and treatment of OSCC.
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