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Article

Pristimerin induces apoptosis of oral squamous cell carcinoma cells via G1 phase arrest and MAPK/Erk1/2 and Akt signaling inhibition

  • Authors:
    • Haiyan Wu
    • Long Li
    • Zhengdong Ai
    • Jingyi Yin
    • Li Chen
  • View Affiliations / Copyright

    Affiliations: Department of Pathophysiology, Medical School, Kunming University of Science and Technology, Kunming, Yunnan 650500, P.R. China, Department of Stomatology, Shekou People's Hospital, Shenzhen, Guangdong 518067, P.R. China
  • Pages: 3017-3025
    |
    Published online on: January 8, 2019
       https://doi.org/10.3892/ol.2019.9903
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Abstract

Pristimerin is an active compound isolated from the traditional Chinese herbs Celastraceae and Hippocrateaceae. It has been reported to exert antitumor effects under experimental and clinical conditions; however, the antitumor effects and underlying mechanisms of pristimerin in oral cancer cells have not yet been identified. In the present study, the anticancer potential of pristimerin was investigated in two oral squamous cell carcinoma (OSCC) cell lines, CAL‑27 and SCC‑25. Results demonstrated that pristimerin was toxic against the two cell lines, and exhibited inhibitory effects against proliferation. Furthermore, pristimerin exhibited a more potent anti‑proliferative activity in CAL‑27 and SCC‑25 cells than the common chemotherapy drugs cisplatin and 5‑fluorouracil. In addition, cell cycle distribution analysis revealed that G0/G1 phase arrest was induced following pristimerin treatment in CAL‑27 and SCC‑25 cells, which was strongly associated with upregulation of p21 and p27, coupled with downregulation of cyclin D1 and cyclin E. Meanwhile, pristimerin induced significant apoptosis of CAL‑27 and SCC‑25 cells, alongside decreased levels of caspase‑3 and specific cleavage of poly (ADP‑ribose) polymerase. These effects were associated with inhibition of the mitogen‑activated protein kinase/extracellular signal‑regulated kinase 1/2 and protein kinase B signaling pathways. With regards to these results, pristimerin may be considered a potent novel active substance for the treatment of OSCC.
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Copy and paste a formatted citation
Spandidos Publications style
Wu H, Li L, Ai Z, Yin J and Chen L: Pristimerin induces apoptosis of oral squamous cell carcinoma cells via G1 phase arrest and MAPK/Erk1/2 and Akt signaling inhibition. Oncol Lett 17: 3017-3025, 2019.
APA
Wu, H., Li, L., Ai, Z., Yin, J., & Chen, L. (2019). Pristimerin induces apoptosis of oral squamous cell carcinoma cells via G1 phase arrest and MAPK/Erk1/2 and Akt signaling inhibition. Oncology Letters, 17, 3017-3025. https://doi.org/10.3892/ol.2019.9903
MLA
Wu, H., Li, L., Ai, Z., Yin, J., Chen, L."Pristimerin induces apoptosis of oral squamous cell carcinoma cells via G1 phase arrest and MAPK/Erk1/2 and Akt signaling inhibition". Oncology Letters 17.3 (2019): 3017-3025.
Chicago
Wu, H., Li, L., Ai, Z., Yin, J., Chen, L."Pristimerin induces apoptosis of oral squamous cell carcinoma cells via G1 phase arrest and MAPK/Erk1/2 and Akt signaling inhibition". Oncology Letters 17, no. 3 (2019): 3017-3025. https://doi.org/10.3892/ol.2019.9903
Copy and paste a formatted citation
x
Spandidos Publications style
Wu H, Li L, Ai Z, Yin J and Chen L: Pristimerin induces apoptosis of oral squamous cell carcinoma cells via G1 phase arrest and MAPK/Erk1/2 and Akt signaling inhibition. Oncol Lett 17: 3017-3025, 2019.
APA
Wu, H., Li, L., Ai, Z., Yin, J., & Chen, L. (2019). Pristimerin induces apoptosis of oral squamous cell carcinoma cells via G1 phase arrest and MAPK/Erk1/2 and Akt signaling inhibition. Oncology Letters, 17, 3017-3025. https://doi.org/10.3892/ol.2019.9903
MLA
Wu, H., Li, L., Ai, Z., Yin, J., Chen, L."Pristimerin induces apoptosis of oral squamous cell carcinoma cells via G1 phase arrest and MAPK/Erk1/2 and Akt signaling inhibition". Oncology Letters 17.3 (2019): 3017-3025.
Chicago
Wu, H., Li, L., Ai, Z., Yin, J., Chen, L."Pristimerin induces apoptosis of oral squamous cell carcinoma cells via G1 phase arrest and MAPK/Erk1/2 and Akt signaling inhibition". Oncology Letters 17, no. 3 (2019): 3017-3025. https://doi.org/10.3892/ol.2019.9903
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