Purpose: To explore the effects of aspirin on the proliferation and apoptosis of human pancreatic cancer cells and its potential molecular mechanism.
Methods: This study included patients with pancreatic cancer who were divided into experimental group and control group. The cell proliferation ability was detected via cell counting kit-8 (CCK-8) assay and colony forming ability via colony formation assay. In addition, changes in proteins in the phosphatidyl inositol-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway were assessed using Western blotting, and rescue experiment was conducted to investigate whether aspirin can affect cell proliferation by inhibiting the PI3K/Akt/mTOR signaling pathway.
Results: The results of CCK-8 assay showed that the proliferation rate of PANC-1 cells was decreased in a time- and dose-dependent manner after they were treated with aspirin at different concentrations. Colony formation assay confirmed that cell colony forming ability was significantly reduced with the increase in aspirin treatment concentration (p<0.05). Besides, the apoptosis rate and the number of cells in the experimental group were higher and larger than those in the control group (p<0.05). According to Western blotting results, the protein expressions of PI3K, phosphorylated (p)-Akt and p-mTOR were decreased after aspirin treatment. Rescue experimental results manifested that insulin-like growth factor 1 (IGF-1) supplementation remarkably elevated the expressions of PI3K, p-Akt and p-mTOR compared with phosphate-buffered saline (PBS) supplementation. It was found in CCK-8 assay that IGF-1 supplementation markedly reversed the inhibition of aspirin on the proliferation of PANC-1 cells in comparison with PBS supplementation.
Conclusions: Aspirin inhibits the proliferation and promotes the apoptosis of pancreatic cancer cells by inactivating the PI3K/Akt/mTOR signaling pathway.