LAUSR

Aspirin may exhibit antitumor activities, as it is able to inhibit cell proliferation. However, the ability of aspirin to inhibit cellular proliferation in Hep-2 cells and its underlying molecular mechanisms have been poorly determined. The aim of the present study was to investigate whether aspirin may induce cell apoptosis in the neoplastic cell line Hep-2. The effects of aspirin on the migratory and invasive abilities of Hep-2 cells were also investigated using Transwell assays. In the present study, it was demonstrated that aspirin induced apoptosis and inhibited proliferation, migration and invasion in Hep-2 cells. Aspirin also significantly decreased the expression of B-cell lymphoma 2 (Bcl-2) and caspase-3, and increased the expression of Bcl-2-associated X protein, suggesting that aspirin induced apoptosis through the intrinsic apoptotic pathway. Hep-2 cells treated with aspirin exhibited a significant upregulation of phosphatase and tensin homolog (PTEN) and decreased levels of phosphorylated protein kinase B (AKT). However, the total amount of AKT protein was not altered in response to aspirin treatment. Furthermore, the expression of nuclear factor (NF)-κB and survivin, which are the downstream targets of the PTEN/AKT signaling pathway, was inhibited. These results indicated that the molecular mechanism underlying the antitumor effects of aspirin may be associated with the inhibition of tumor invasion and induction of apoptosis by regulating the activity of the PTEN/AKT/NF-κB/survivin signaling pathway.