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)-, 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.