LASS2 overexpression enhances early apoptosis of lung cancer cells through the caspase‑dependent pathway

In a previous study by the authors, the longevity assurance homolog 2 ( ) gene was determined to inhibit activity of vacuolar H ‑ATPase (V‑ATPase) by combining with the C subunit (ATP6L) of V‑ATPase. However, the influence of overexpression and silencing on apoptosis of human lung cancer cells 95D or 95C remains unclear. Thus, the effect of on apoptosis and its potential mechanisms were investigated in 95D and 95C cells. Using the lentiviral transfection method, lentiviral vectors of overexpression and silencing were transfected into 95D and 95C cells, respectively. The apoptotic ability of tumor cells was observed by flow cytometry. The expression levels of , Bcl‑2, Bax, cytochrome , caspase‑9, and caspase‑3 were detected by western blotting. CCK‑8 assay was used to detect the growth ability of tumor cells . Flow cytometric analysis revealed that overexpression could promote the early apoptosis of lung cancer cells 95D. CCK‑8 assay demonstrated that overexpression inhibited the proliferation of 95D cells. Additionally, overexpression decreased the expression of Bcl‑2, induced the release of cytochrome from mitochondria, and promoted the activation of caspase‑9 and caspase‑3. There was a significant difference in the expression of Bcl‑2, cytochrome , caspase‑9 and caspase‑3 in the ‑overexpression group compared with the normal and negative control groups. Alternatively, the aforementioned experiments in lung cancer cells 95C following silencing produced the opposite effects. may induce early apoptosis of lung cancer cells by influencing the caspase‑dependent mitochondrial pathway.