Antitumor effects of dioscin in A431 cells via adjusting ATM/p53‑mediated cell apoptosis, DNA damage and migration

Skin cancer is the deadliest type of malignant disease and causes primary mortality worldwide. Dioscin, which exists in medicinal plants, has potent anticancer effects. However, its effects on skin cancer remain unknown. In the present study, the activity and mechanism of dioscin on the human skin c...

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Bibliographic Details
Published in:Oncology letters 2021-01, Vol.21 (1), p.1-59, Article 59
Main Authors: Wang, Peng, And, Chun Wang, Liu, Chunying
Format: Article
Language:English
Subjects:
Analysis
Apoptosis
Cancer
Cancer therapies
Care and treatment
Cell adhesion & migration
Cell cycle
Computer software industry
Deoxyribonucleic acid
DNA
DNA damage
Health aspects
Herbal medicine
Instrument industry
Investigations
Kinases
Mediation
Medicinal plants
Medicine, Botanic
Medicine, Herbal
Melanoma
Metastasis
Natural products
Penicillin
RNA
Skin
Skin cancer
Tumor proteins
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Summary:Skin cancer is the deadliest type of malignant disease and causes primary mortality worldwide. Dioscin, which exists in medicinal plants, has potent anticancer effects. However, its effects on skin cancer remain unknown. In the present study, the activity and mechanism of dioscin on the human skin cancer A431 cell line were investigated, MTT, colony formation, Transwell, wound-healing, TUNEL, Comet, immunofluorescence and western blot assays were used to assess the effects of dioscin on A431 cells. The results of MTT, colony formation, Transwell and wound-healing assays revealed that dioscin suppressed proliferation, colony formation and invasion of the cancer cells. TUNEL and comet assays demonstrated that dioscin exhibited significant effects on cell apoptosis and DNA damage. Investigations into the mechanism revealed that the expression levels of phosphorylated Ataxia telangiectasia-mutated (ATM) were considerably activated by dioscin, which significantly upregulated the expression levels of p53 to activate mitochondrial apoptosis signaling. Furthermore, the expression levels of BAX, cleaved caspase-3/9 and cleaved poly (ADP-ribose) polymerase were upregulated, and the expression levels of BCL-2 were downregulated by dioscin. Additionally, dioscin markedly downregulated the expression levels of matrix metalloproteinase 2 (MMP2), MMP9, RHO and cdc42, which are all associated with tumor invasion. In addition, p53-small interfering RNA transfection experiments indicated that dioscin exhibited excellent activity against skin cancer in vitro by decreasing p53 expression. Overall, the present results suggested that dioscin inhibited skin cancer cell proliferation via adjusting ATM/p53-mediated cell apoptosis, migration and DNA damage, which should be considered as a potential option for future treatments of skin cancer. Key words: dioscin, skin cancer, p53 signal, cell apoptosis, DNA damage
ISSN:1792-1074
1792-1082
DOI:10.3892/ol.2020.12321