Tripterine enhances regulatory effect of TNF-α on Caspase-3 and induces apoptosis of lung cancer cell
Lung cancer is a common malignancy of the respiratory system with a high morbidity and mortality. We intended to identify the apoptosis-promoting role of tripterine in lung cancer. Lung cancer SPC-A-1 cells were exposed to low, moderate, and high dosage of tripterine (2, 5 and 10 μmol/L) with the model group not being intervened. After treatment, the role of tripterine in SPC-A-1 cell apoptosis was observed. In addition, lung cancer cells were transfected with TNF-α mimic (pc-TNF-α group) and TNF-α inhibitor (si-TNF-α group). Tripterine +pc-TNF-α group was set up to determine the interaction between tripterine and TNF-α. The cell survival rate, TNF-α and Caspase-3 expression levels then were detected by MTT and flow cytometry. Tripteryglide treatment dose-dependently decreased lung cancer cell viability and induced cell apoptosis, resulting in an increase of TNF-α expression. However, when TNF-α expression was inhibited upon transfection, SPC-A-1 cell apoptosis was suppressed. TNF-α mimics activated apoptosis and up-regulated Caspase-3 expression. Combination of tripteryglide and TNF-α mimics more significantly elevated apoptotic rate of lung cancer cells when elevating the content of Caspase-3. SPC-A-1 cells are highly sensitive to TNF-α and TNF-α significantly increases the activity and expression of Caspase-3. Tripteryglide can up-regulate TNF-α expression to facilitate lung cancer cell apoptosis and increase Caspase-3 expression.
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