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

Abstract

In a previous study by the authors, the longevity assurance homolog 2 (LASS2) 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 LASS2 overexpression and silencing on apoptosis of human lung cancer cells 95D or 95C remains unclear. Thus, the effect of LASS2 on apoptosis and its potential mechanisms were investigated in 95D and 95C cells. Using the lentiviral transfection method, lentiviral vectors of LASS2 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 LASS2, Bcl‑2, Bax, cytochrome c, caspase‑9, and caspase‑3 were detected by western blotting. CCK‑8 assay was used to detect the growth ability of tumor cells invitro. Flow cytometric analysis revealed that LASS2 overexpression could promote the early apoptosis of lung cancer cells 95D. CCK‑8 assay demonstrated that LASS2 overexpression inhibited the proliferation of 95D cells. Additionally, LASS2 overexpression decreased the expression of Bcl‑2, induced the release of cytochrome c from mitochondria, and promoted the activation of caspase‑9 and caspase‑3. There was a significant difference in the expression of Bcl‑2, cytochrome c, caspase‑9 and caspase‑3 in the LASS2‑overexpression group compared with the normal and negative control groups. Alternatively, the aforementioned experiments in lung cancer cells 95C following LASS2 silencing produced the opposite effects. LASS2 may induce early apoptosis of lung cancer cells by influencing the caspase‑dependent mitochondrial pathway.