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

  • Authors:
    • Peng Wang
    • Chun Wang
    • Chunying Liu
  • View Affiliations / Copyright

    Affiliations: College of Pharmacy, Liaoning University of Traditional Chinese Medicine, Shenyang, Liaoning 110847, P.R. China
    Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 59
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    Published online on: November 19, 2020
       https://doi.org/10.3892/ol.2020.12321
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Abstract

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.
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Copy and paste a formatted citation
Spandidos Publications style
Wang P, Wang C and Liu C: Antitumor effects of dioscin in A431 cells via adjusting ATM/p53‑mediated cell apoptosis, DNA damage and migration. Oncol Lett 21: 59, 2021.
APA
Wang, P., Wang, C., & Liu, C. (2021). Antitumor effects of dioscin in A431 cells via adjusting ATM/p53‑mediated cell apoptosis, DNA damage and migration. Oncology Letters, 21, 59. https://doi.org/10.3892/ol.2020.12321
MLA
Wang, P., Wang, C., Liu, C."Antitumor effects of dioscin in A431 cells via adjusting ATM/p53‑mediated cell apoptosis, DNA damage and migration". Oncology Letters 21.1 (2021): 59.
Chicago
Wang, P., Wang, C., Liu, C."Antitumor effects of dioscin in A431 cells via adjusting ATM/p53‑mediated cell apoptosis, DNA damage and migration". Oncology Letters 21, no. 1 (2021): 59. https://doi.org/10.3892/ol.2020.12321
Copy and paste a formatted citation
x
Spandidos Publications style
Wang P, Wang C and Liu C: Antitumor effects of dioscin in A431 cells via adjusting ATM/p53‑mediated cell apoptosis, DNA damage and migration. Oncol Lett 21: 59, 2021.
APA
Wang, P., Wang, C., & Liu, C. (2021). Antitumor effects of dioscin in A431 cells via adjusting ATM/p53‑mediated cell apoptosis, DNA damage and migration. Oncology Letters, 21, 59. https://doi.org/10.3892/ol.2020.12321
MLA
Wang, P., Wang, C., Liu, C."Antitumor effects of dioscin in A431 cells via adjusting ATM/p53‑mediated cell apoptosis, DNA damage and migration". Oncology Letters 21.1 (2021): 59.
Chicago
Wang, P., Wang, C., Liu, C."Antitumor effects of dioscin in A431 cells via adjusting ATM/p53‑mediated cell apoptosis, DNA damage and migration". Oncology Letters 21, no. 1 (2021): 59. https://doi.org/10.3892/ol.2020.12321
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