Aim:
Background: Lung cancer is one of the primary causes of cancer-related death. The effectiveness of current treatments is frequently hampered by side effects, medication resistance. Dipeptidyl peptidase-4 (DPP-4) inhibitors, which are mainly used to treat diabetes, have shown promising anticancer properties in a variety of cancer types. Aim: To evaluate the anticancer, apoptotic, and antioxidant effects of Alo on A549 cells, both alone and in combination with CP, and to elucidate the molecular mechanisms underlying the death of cancer cells.

Material and methods:
Materials & Methods: The American Type Culture Collection's (ATCC) normal HBL100 cells and human lung A549 cells were used in the investigation. The cells were split into four groups. Following a 72-hour incubation period, ELISA assays were used to quantify the levels of the DPP-4 enzyme, apoptotic regulators (Bax and caspase-3), and oxidative stress marker (malondialdehyde) in lung cancer cell and normal cell lines. One-way ANOVA with significance set at P < 0.05 were used in the statistical analysis.

Results:
Results: The findings showed that Alo reduced the activity of the DPP-4 enzyme in both cell lines (P < 0.0001). Molecular analysis showed a considerable increase in pro-apoptotic markers (BAX, Caspase-3). Higher amounts of malondialdehyde were indicative of increased oxidative stress in both monotherapy and combination. But in HBL 100 cells, Alo decreased BAX, caspase-3, and MDA levels.

Conclusions:
Conclusion: Alo has caused cancer cell death through a variety of mechanisms, such as DPP4 inhibition, apoptotic pathway activation, and oxidative stress enhancement based on DPP-4, BAX, caspase-3, and MDA measurements.