Gao Tangxin, Zheng Shangyong, Li Qian, Ran Pengzhan, Sun Lijuan, Yuan Yuncang, Xiao Chunjie
School of Medicine, Yunnan University, Kunming, Yunnan 650091, P.R. China.
Key Laboratory of Molecular Genetics of Human Complicated Diseases, Department of Education, Kunming, Yunnan 650091, P.R. China.
Oncol Rep. 2015 Nov;34(5):2333-42. doi: 10.3892/or.2015.4245. Epub 2015 Sep 2.
The eyes absent homologue 2 (EYA2) is a dual-functional transcription factor/phosphatase that plays a critical role in neoplasia. The precise effects of EYA2 remain elusive in non-small cell lung cancer (NSCLC). In the present study, we examined EYA2 expression in NSCLC cell lines and a normal pulmonary epithelial cell line. We found that EYA2 was aberrantly upregulated in the lung adenocarcinoma cells. Therefore, we studied the methylation status of the eya2 gene in a lung adenocarcinoma cell line, a normal pulmonary epithelial cell line and lung adenocarcinoma tissues. Furthermore, the eya2 gene was knocked down in lung adenocarcinoma cells via RNA interference to investigate the regulatory role of EYA2; specifically, cell proliferation, cell cycle distribution, apoptosis, migration and invasive capacities were assessed in tje EYA2‑knockdown cancer cells. The results showed that the aberrant hypomethylation and overexpression of the eya2 gene were associated with lung adenocarcinoma oncogenesis. In addition, inhibition of EYA2 expression suppressed tumour cell growth by altering the proliferation, cell cycle distribution, apoptosis, migration and invasive capacities of the cells. These findings demonstrated that EYA2 functions as a stimulant in lung adenocarcinoma pathogenesis and may facilitate the development of novel diagnostic targets and therapy strategies for lung adenocarcinoma.
眼缺失同源物2（EYA2）是一种双功能转录因子/磷酸酶，在肿瘤形成中起关键作用。EYA2在非小细胞肺癌（NSCLC）中的精确作用仍不清楚。在本研究中，我们检测了NSCLC细胞系和正常肺上皮细胞系中EYA2的表达。我们发现EYA2在肺腺癌细胞中异常上调。因此，我们研究了肺腺癌细胞系、正常肺上皮细胞系和肺腺癌组织中eya2基因的甲基化状态。此外，通过RNA干扰在肺腺癌细胞中敲低eya2基因以研究EYA2的调节作用；具体而言，在EYA2敲低的癌细胞中评估细胞增殖、细胞周期分布、凋亡、迁移和侵袭能力。结果表明，eya2基因的异常低甲基化和过表达与肺腺癌的发生有关。此外，抑制EYA2表达可通过改变细胞的增殖、细胞周期分布、凋亡、迁移和侵袭能力来抑制肿瘤细胞生长。这些发现表明，EYA2在肺腺癌发病机制中起刺激作用，并可能有助于开发新的肺腺癌诊断靶点和治疗策略。
