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Article

Docosahexaenoic acid inhibits the phosphorylation of STAT3 and the growth and invasion of renal cancer cells

  • Authors:
    • Shinsuke Tasaki
    • Akio Horiguchi
    • Takako Asano
    • Keiichi Ito
    • Tomohiko Asano
    • Hirotaka Asakura
  • View Affiliations / Copyright

    Affiliations: Department of Urology, National Defense Medical College, Tokorozawa, Saitama 359‑8513, Japan, Department of Urology, Saitama Medical University, Moroyama, Saitama 350‑0495, Japan
  • Pages: 1146-1152
    |
    Published online on: June 15, 2017
       https://doi.org/10.3892/etm.2017.4616
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Abstract

Docosahexaenoic acid (DHA) has a variety of anti‑tumor activities. The present study examined the anti‑tumor activity of DHA in renal cancer cells and its underlying mechanisms of action. The effects of DHA on the viability and proliferation of the human renal cancer cell lines Caki‑1 and 786‑O were examined by an MTS assay and cell counting. In addition, cell cycle distribution and cell apoptosis were analyzed by flow cytometry and Annexin V staining, and modulation of cell mobility and invasiveness was assessed by wound healing and Matrigel invasion assays. Effects of DHA on intracellular signaling pathways were also analyzed by western blotting. It was observed that DHA significantly reduced the viability and proliferation of Caki‑1 and 786‑O cells (P<0.01). Specifically, there were increases in the sub‑G1 and G2/M cell populations, as well as the percentages of cells exhibiting Annexin‑positive and propidium‑iodide‑negative staining. In addition, the covered area in a wound and the number of cells invading through a Matrigel chamber decreased when Caki‑1 or 786‑O cells were treated with DHA. Phosphorylation of epidermal growth factor receptor was also upregulated following DHA treatment, while phosphorylation of signal transducer and activator of transcription 3 and Akt was downregulated. Collectively, these data suggest that DHA may be useful in the treatment of renal cell carcinoma.
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Copy and paste a formatted citation
Spandidos Publications style
Tasaki S, Horiguchi A, Asano T, Ito K, Asano T and Asakura H: Docosahexaenoic acid inhibits the phosphorylation of STAT3 and the growth and invasion of renal cancer cells. Exp Ther Med 14: 1146-1152, 2017.
APA
Tasaki, S., Horiguchi, A., Asano, T., Ito, K., Asano, T., & Asakura, H. (2017). Docosahexaenoic acid inhibits the phosphorylation of STAT3 and the growth and invasion of renal cancer cells. Experimental and Therapeutic Medicine, 14, 1146-1152. https://doi.org/10.3892/etm.2017.4616
MLA
Tasaki, S., Horiguchi, A., Asano, T., Ito, K., Asano, T., Asakura, H."Docosahexaenoic acid inhibits the phosphorylation of STAT3 and the growth and invasion of renal cancer cells". Experimental and Therapeutic Medicine 14.2 (2017): 1146-1152.
Chicago
Tasaki, S., Horiguchi, A., Asano, T., Ito, K., Asano, T., Asakura, H."Docosahexaenoic acid inhibits the phosphorylation of STAT3 and the growth and invasion of renal cancer cells". Experimental and Therapeutic Medicine 14, no. 2 (2017): 1146-1152. https://doi.org/10.3892/etm.2017.4616
Copy and paste a formatted citation
x
Spandidos Publications style
Tasaki S, Horiguchi A, Asano T, Ito K, Asano T and Asakura H: Docosahexaenoic acid inhibits the phosphorylation of STAT3 and the growth and invasion of renal cancer cells. Exp Ther Med 14: 1146-1152, 2017.
APA
Tasaki, S., Horiguchi, A., Asano, T., Ito, K., Asano, T., & Asakura, H. (2017). Docosahexaenoic acid inhibits the phosphorylation of STAT3 and the growth and invasion of renal cancer cells. Experimental and Therapeutic Medicine, 14, 1146-1152. https://doi.org/10.3892/etm.2017.4616
MLA
Tasaki, S., Horiguchi, A., Asano, T., Ito, K., Asano, T., Asakura, H."Docosahexaenoic acid inhibits the phosphorylation of STAT3 and the growth and invasion of renal cancer cells". Experimental and Therapeutic Medicine 14.2 (2017): 1146-1152.
Chicago
Tasaki, S., Horiguchi, A., Asano, T., Ito, K., Asano, T., Asakura, H."Docosahexaenoic acid inhibits the phosphorylation of STAT3 and the growth and invasion of renal cancer cells". Experimental and Therapeutic Medicine 14, no. 2 (2017): 1146-1152. https://doi.org/10.3892/etm.2017.4616
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