Open Access

Icariin inhibits oral squamous cell carcinoma cell proliferation and induces apoptosis via inhibiting the NF‑κB and PI3K/AKT pathways

  • Authors:
    • Ling Sun
    • Jing Zhang
  • View Affiliations

  • Published online on: July 1, 2021     https://doi.org/10.3892/etm.2021.10374
  • Article Number: 942
  • Copyright: © Sun et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Oral squamous cell carcinoma (OSCC), one of the most common types of human cancer, has a high mortality rate and a poor prognosis due to its high rates of recurrence and metastasis. In recent years, icariin (ICA) has been reported to play an important role in a variety of malignancies, such as gastric, colorectal, pancreatic and ovarian cancer. However, its role and mechanism in OSCC remains to be elucidated. The present study aimed to investigate the effect of ICA in OSCC cells and to reveal its underlying mechanisms. The OSCC cell lines SCC9 and Cal 27 were used to explore the effect of different concentrations of ICA on the biological behavior of OSCC cells. The effect of ICA on OSCC cell proliferation and apoptosis was determined using 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyl‑2H‑tetrazolium bromide and flow cytometric assays, respectively. Subsequently, the protein expression levels of caspase‑3 and cleaved‑caspase‑3 were detected using western blot analysis. Additionally, the protein and mRNA expression levels of nuclear factor‑κB (NF‑κB) and phosphatidylinositol‑3‑kinase (PI3K)/protein kinase B (AKT) signaling pathway‑related factors were determined using western blot analysis and reverse transcription‑quantitative PCR, respectively. The results demonstrated that ICA inhibited OSCC cell proliferation and significantly increased the apoptosis rate in a dose‑dependent manner. In addition, treatment of OSCC cells with ICA upregulated the protein expression of cleaved‑caspase‑3 and increased the cleaved‑caspase‑3/caspase‑3 ratio. The protein expression levels of phosphorylated (p)‑p65, p‑PI3K and p‑AKT were decreased in OSCC cells treated with ICA. The aforementioned findings revealed that ICA could attenuate the proliferation of OSCC cells and induce apoptosis via inhibiting the NF‑κB and PI3K/AKT signaling pathways. Therefore, the current study provided a new insight into the clinical treatment of OSCC.
View Figures
View References

Related Articles

Journal Cover

September-2021
Volume 22 Issue 3

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Sun L and Sun L: Icariin inhibits oral squamous cell carcinoma cell proliferation and induces apoptosis via inhibiting the NF‑κB and PI3K/AKT pathways. Exp Ther Med 22: 942, 2021
APA
Sun, L., & Sun, L. (2021). Icariin inhibits oral squamous cell carcinoma cell proliferation and induces apoptosis via inhibiting the NF‑κB and PI3K/AKT pathways. Experimental and Therapeutic Medicine, 22, 942. https://doi.org/10.3892/etm.2021.10374
MLA
Sun, L., Zhang, J."Icariin inhibits oral squamous cell carcinoma cell proliferation and induces apoptosis via inhibiting the NF‑κB and PI3K/AKT pathways". Experimental and Therapeutic Medicine 22.3 (2021): 942.
Chicago
Sun, L., Zhang, J."Icariin inhibits oral squamous cell carcinoma cell proliferation and induces apoptosis via inhibiting the NF‑κB and PI3K/AKT pathways". Experimental and Therapeutic Medicine 22, no. 3 (2021): 942. https://doi.org/10.3892/etm.2021.10374