Silencing lncRNA EZR‑AS1 induces apoptosis and attenuates the malignant properties of lung adenocarcinoma cells.

Adenocarcinoma is one of the major subtypes of lung cancer. This study aimed to investigate the effect of silencing long non-coding RNA (lncRNA) EZR‑AS1 on the biological behaviors of lung adenocarcinoma (ADC) cells. EZR‑AS1 expression levels in lung ADC tissues and cells, as well as in adjacent non-cancerous tissues, were determined using quantitative reverse transcription polymerase chain reaction (qRT-PCR). EZR‑AS1 was knocked down in two lung ADC cell lines using small interfering RNA specific for EZR‑AS1 (siEZR‑AS1). Proliferation, migration, and apoptosis of EZR‑AS1-knockdown cells were assessed using the CCK-8 viability assay, flow cytometry, or wound healing experiments. The levels of proteins related to migration pathways were evaluated using western blotting analysis. EZR‑AS1 contents were significantly higher in lung ADC tissues and cells than in the levels in the non-cancerous tissues and cells (p<0.01). Transfection of ADC cell lines H1437 and H1975 significantly downregulated EZR‑AS1 levels in both cell lines. Cytotoxicity assays revealed that the viability of EZR‑AS1-knockdown cells significantly decreased over culture time, and a significant level of apoptosis was induced (p<0.01). Wounding healing experiments revealed that EZR‑AS1-knockdown significantly reduced the migration rate of both cell lines (p<0.01). Furthermore, proteins related to migration pathways such as vimentin, MMP2, and MMP9 were significantly downregulated, whereas the E-cadherin level was significantly increased after EZR‑AS1 knockdown. Our work demonstrated that EZR-AS1 is associated with ADC progression, and silencing this gene inhibits proliferation and reduces migration of ADC cells in vitro. The altered expression of metastasis-related genes was likely responsible for the reduced migration ability after EZR-AS1 knockdown.