腺癌是肺癌的主要亚型之一。本研究旨在调查沉默长非编码RNA（lncRNA）EZR-AS1对肺腺癌（ADC）细胞的生物行为的影响。使用定量逆转录聚合酶链反应（qRT-PCR）测定肺ADC组织和细胞，以及相邻非癌组织中的EZR-AS1表达水平。使用特异性靶向EZR-AS1的小干扰RNA（siEZR-AS1）在两种肺ADC细胞系中敲低EZR-AS1。使用CCK-8活力分析、流式细胞术或创伤愈合实验评估EZR-AS1敲低细胞的增殖、迁移和凋亡情况。使用西方博蛋白免疫印记分析评估与迁移途径相关的蛋白水平。与非癌组织和细胞相比，肺ADC组织和细胞中的EZR-AS1含量显著升高（p<0.01）。转染ADC细胞系H1437和H1975使两种细胞系中EZR-AS1水平显著下调。细胞毒性分析显示，EZR-AS1敲低细胞的存活率随培养时间显著降低，并引发显著的凋亡（p<0.01）。创伤愈合实验表明，EZR-AS1敲低显著降低了两种细胞系的迁移率（p<0.01）。此外，在EZR-AS1敲低后，与迁移途径相关的蛋白如vimentin、MMP2和MMP9显著下调，而E-cadherin水平显著上调。我们的研究表明，EZR-AS1与ADC进展相关，沉默该基因抑制了ADC细胞的增殖并降低了其体外迁移能力。在EZR-AS1敲低后，转移相关基因的表达变化可能是减少迁移能力的原因。

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.