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ESE1 suppresses the growth, invasion and migration of human NSCLC cells and tumor formation in vivo

Authors
Lou, Z; Lee, BS; Ha, T; Xu, Y; Kim, HJ; Kim, CH; Lee, SH
Citation
Oncology reports, 40(3):1734-1742, 2018
Journal Title
Oncology reports
ISSN
1021-335X1791-2431
Abstract
Lung cancer is the first leading cause of cancerrelated death in the United States. Nonsmall 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. Epithelialspecific ETS1 (ESE1) belongs to the superfamily of ETS transcription factors. The effect of ESE1 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 ESE1 expression affects tumorigenic activity using human NSCLC cells and a mouse xenograft model. ESE1 expression suppressed anchorageindependent growth in soft agar assay and led to an increase in G1 arrest and apoptosis in human NSCLC cells. ESE1 expression suppressed the invasion and migration of human NSCLC cells. Western blot analysis, RTPCR and promoter assay indicated that ESE1 expression was transcriptionally downregulated by treatment of transforming growth factor (TGF)beta, an EMT (epithelialmesenchymal transition) stimulator. The xenograft study indicated that ESE1 expression inhibited tumor formation and development. Our data demonstrated that ESE1 plays a key role as a tumor suppressor in human NSCLC.
Keywords
ESE-1tumorigenesisEMTxenograftNSCLC
MeSH terms
AnimalsApoptosisBiomarkers, Tumor/metabolism*CarcinogenesisCarcinoma, Non-Small-Cell Lung/metabolismCarcinoma, Non-Small-Cell Lung/pathology*Cell Movement*Cell Proliferation*DNA-Binding Proteins/metabolism*Epithelial-Mesenchymal TransitionHumansLung Neoplasms/metabolismLung Neoplasms/pathology*MaleMiceMice, Inbred BALB CMice, NudeNeoplasm InvasivenessProto-Oncogene Proteins c-ets/metabolism*Signal TransductionTranscription Factors/metabolism*Transforming Growth Factor beta/metabolism*Tumor Cells, CulturedXenograft Model Antitumor Assays
DOI
10.3892/or.2018.6560
PMID
30015943
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Otolaryngology
AJOU Authors
이, 복순김, 철호
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