ESE‑1 suppresses the growth, invasion and migration of human NSCLC cells and tumor formation in vivo.

Lung cancer is the first leading cause of cancer‑related death in the United States. Non‑small cell lung cancer (NSCLC) is the most common type of lung cancer and is associated with a poor patient prognosis. Identification of promising molecular targets is required for the effective prevention and therapy of NSCLC. Epithelial‑specific ETS‑1 (ESE‑1) belongs to the superfamily of ETS transcription factors. The effect of ESE‑1 on tumorigenesis is controversial in several types of cancer while its role in lung cancer remains unknown. The present study was designed to investigate whether ESE‑1 expression affects tumorigenic activity using human NSCLC cells and a mouse xenograft model. ESE‑1 expression suppressed anchorage‑independent growth in soft agar assay and led to an increase in G1 arrest and apoptosis in human NSCLC cells. ESE‑1 expression suppressed the invasion and migration of human NSCLC cells. Western blot analysis, RT‑PCR and promoter assay indicated that ESE‑1 expression was transcriptionally downregulated by treatment of transforming growth factor (TGF)‑β, an EMT (epithelial‑mesenchymal transition) stimulator. The xenograft study indicated that ESE‑1 expression inhibited tumor formation and development. Our data demonstrated that ESE‑1 plays a key role as a tumor suppressor in human NSCLC.