Open Access

Polydatin inhibits hepatocellular carcinoma via the AKT/STAT3‑FOXO1 signaling pathway

Corrigendum in: /10.3892/ol.2019.10856

  • Authors:
    • Jian Jiang
    • Yaodong Chen
    • Tianxiu Dong
    • Minlu Yue
    • Yu Zhang
    • Tingting An
    • Jiuwei Zhang
    • Pengfei Liu
    • Xiuhua Yang
  • View Affiliations

  • Published online on: March 7, 2019     https://doi.org/10.3892/ol.2019.10123
  • Pages: 4505-4513
  • Copyright: © Jiang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Polydatin, extracted from Polygonum cuspidatum, is known for its anti‑platelet aggregation and anti‑inflammatory effects. However, studies on the association of polydatin with cancer are limited, particularly with regards to epithelial‑mesenchymal transition (EMT)‑associated migration and invasion of cancer cells. The purpose of the present study was to reveal the potential anticancer effects of polydatin on hepatocellular carcinoma (HCC) cells, particularly its effects on EMT. MTT assay was used to determine cell viability. Migration and invasion were evaluated through wound healing and transwell assays. Colony formation efficiency assay was conducted to detect proliferation. Flow cytometric analyses of apoptosis and cell cycle progression were performed following cells staining with Annexin V‑fluorescein isothiocyanate (FITC)/propidium iodide (PI) and PI alone, respectively. Western blotting was used to investigate relevant molecular mechanisms. The results indicated that polydatin inhibited proliferation via G2/M arrest, suppressed migration and invasion of HCC cells, and promoted their apoptosis. In addition, phosphorylated (p)‑protein kinase B (AKT), p‑Janus kinase 1 and p‑signal transducer and activator of transcription 3 (STAT3) levels were decreased as polydatin concentrations increased, and forkhead box protein O1 (FOXO1) expression was upregulated. Furthermore, the expression levels of various markers of EMT were reversed following treatment with polydatin. In conclusion, the present study validated that polydatin may inhibit proliferation via G2/M arrest, and suppressed EMT‑associated migration and invasion of HCC cells. The results also suggested that polydatin may promote HCC cell apoptosis by blocking the AKT/STAT3‑FOXO1 signaling pathway.
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May-2019
Volume 17 Issue 5

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Copy and paste a formatted citation
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Spandidos Publications style
Jiang J, Chen Y, Dong T, Yue M, Zhang Y, An T, Zhang J, Liu P and Yang X: Polydatin inhibits hepatocellular carcinoma via the AKT/STAT3‑FOXO1 signaling pathway Corrigendum in /10.3892/ol.2019.10856. Oncol Lett 17: 4505-4513, 2019
APA
Jiang, J., Chen, Y., Dong, T., Yue, M., Zhang, Y., An, T. ... Yang, X. (2019). Polydatin inhibits hepatocellular carcinoma via the AKT/STAT3‑FOXO1 signaling pathway Corrigendum in /10.3892/ol.2019.10856. Oncology Letters, 17, 4505-4513. https://doi.org/10.3892/ol.2019.10123
MLA
Jiang, J., Chen, Y., Dong, T., Yue, M., Zhang, Y., An, T., Zhang, J., Liu, P., Yang, X."Polydatin inhibits hepatocellular carcinoma via the AKT/STAT3‑FOXO1 signaling pathway Corrigendum in /10.3892/ol.2019.10856". Oncology Letters 17.5 (2019): 4505-4513.
Chicago
Jiang, J., Chen, Y., Dong, T., Yue, M., Zhang, Y., An, T., Zhang, J., Liu, P., Yang, X."Polydatin inhibits hepatocellular carcinoma via the AKT/STAT3‑FOXO1 signaling pathway Corrigendum in /10.3892/ol.2019.10856". Oncology Letters 17, no. 5 (2019): 4505-4513. https://doi.org/10.3892/ol.2019.10123