Conclusion
PRDX1 was highly expressed in esophageal cancer cells. Silencing of PRDX1 can inhibit the proliferation of esophageal cancer cells and promote apoptosis. The mechanism involved in this process may be related to the inhibition of the PI3K/AKT signaling pathway.
Methods
Three esophageal squamous cell carcinoma cell lines (Eca-109, EC9706, and KYSE150) and one normal cell line (human esophageal epithelial cells) were selected. The protein expression of peroxiredoxin 1 (PRDX1) and the activity of the PI3K/AKT pathway were detected via Western blotting. The proliferation ability of cells was detected through the MTT assay and cell clone formation. Apoptosis was detected using flow cytometry. Subsequently, cells were treated with a PI3K/AKT pathway inhibitor and activator, alone or in combination with silencing of PRDX1, and the above indicators were re-tested.
Objective
To study the effect of peroxiredoxin 1 (PRDX1) on esophageal squamous carcinoma cells and determine whether it plays a role in regulating the PI3K/AKT signaling pathway.
Results
The expression of PRDX1 and activity of PI3K/AKT pathway-associated proteins were higher in esophageal cancer cells than in normal esophageal epithelial cells. Compared with normal human esophageal epithelial cells, the proliferation of the three types of esophageal cancer cells was increased, whereas their level of apoptosis was decreased (p<0.05). In Eca-109 cells (cell line with silenced expression of PRDX1), the expression of PRDX1 was significantly decreased. In contrast to the control group, the proliferation and clonality of cells in the silencing PRDX1 group was decreased, the proportion of apoptotic cells was increased, and the phosphorylation levels of PI3K and AKT were decreased (p<0.05). Compared with the control group, treatment with the inhibitor LY294002 alone significantly inhibited cell proliferation and promoted apoptosis (p<0.05); this effect was similar to that observed in the silencing PRDX1 group.