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©The Author(s) 2020.
World J Gastroenterol. Oct 14, 2020; 26(38): 5822-5835
Published online Oct 14, 2020. doi: 10.3748/wjg.v26.i38.5822
Published online Oct 14, 2020. doi: 10.3748/wjg.v26.i38.5822
Figure 4 Effects of phosphatase and tensin homolog /Akt inhibitor on acetyl-11-keto-β-boswellic acid-induced down-regulation of cyclooxygenase-2 expression in gastric cancer cells.
Gastric cells were pre-treated with the phosphatase and tensin homolog (PTEN) inhibitor bpv (HOpic, 17.4 ng/mL, A and B) or Akt inhibitor MK2206 (38.4 ng/mL, C and D) for 30 min and then treated with acetyl-11-keto-β-boswellic acid (40 µM) for 48 h. A: Expression of PTEN, cyclooxygenase (COX)-2, and total and phosphorylated forms of Akt in gastric cancer cells detected by Western blot analysis. B: Histograms showing the relative expression of PTEN and COX-2 compared with GAPDH, and phospho-Akt (p-Akt) compared with total Akt, respectively. Each data point represents the mean ± SD from three independent experiments. aP < 0.05, bP < 0.01 vs Control; cP < 0.05, dP < 0.01 vs AKBA. AKBA: Acetyl-11-keto-β-boswellic acid; PTEN: Phosphatase and tensin homolog; COX-2: Cyclooxygenase-2; GAPDH: Glyceraldehyde-phosphate dehydrogenase.
- Citation: Sun MX, He XP, Huang PY, Qi Q, Sun WH, Liu GS, Hua J. Acetyl-11-keto-β-boswellic acid inhibits proliferation and induces apoptosis of gastric cancer cells through the phosphatase and tensin homolog /Akt/ cyclooxygenase-2 signaling pathway. World J Gastroenterol 2020; 26(38): 5822-5835
- URL: https://www.wjgnet.com/1007-9327/full/v26/i38/5822.htm
- DOI: https://dx.doi.org/10.3748/wjg.v26.i38.5822