Xu Xiaohui, Cao Lei, Zhang Ye, Yin Yan, Hu Xue, Cui Yushang
Department of Thoracic Surgery, Peking Union Medical College Hospital, Beijing 100730, P.R. China.
Graduate School of Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, P.R. China.
Oncol Lett. 2018 Jan;15(1):257-263. doi: 10.3892/ol.2017.7329. Epub 2017 Nov 2.
Lung cancer, a malignant tumor, is the most frequently fatal cancer, with poor survival rates in the advanced stages. In order to improve the understanding of this disease, and to improve the outcomes of patients, additional studies are required. In the present study, differentially expressed genes (DEGs) in patients with lung cancer compared with controls were identified. To understand how these DEGs act together to account for the initiation of lung cancer, a protein interaction network and a transcriptional regulatory network were constructed to explore the clusters and pathways in lung cancer, and the results indicated that PTTG1 and MMP9 served major roles in the development of lung cancer in the regulatory system. Consistent with this, mRNA and protein expression levels of PTTG1 and MMP9 were significantly upregulated in lung cancer tissues compared with normal lung tissues. The overexpression of PTTG1 or MMP9 was induced in the human bronchial epithelial BEAS-2B cell line, indicating that increased PTTG1 or MMP9 alone may not only facilitate cell migration, proliferation and induce colony formation, but also suppress cell apoptosis. In summary, PTTG1 and MMP9 were identified as potential targets for therapeutic intervention through gene therapy in lung cancer.
肺癌是一种恶性肿瘤,是最常见的致命性癌症,晚期生存率很低。为了增进对这种疾病的了解并改善患者的治疗效果,需要进行更多研究。在本研究中,确定了肺癌患者与对照组相比的差异表达基因(DEG)。为了了解这些DEG如何共同作用导致肺癌的发生,构建了蛋白质相互作用网络和转录调控网络以探索肺癌中的簇和通路,结果表明PTTG1和MMP9在调控系统中对肺癌的发展起主要作用。与此一致的是,与正常肺组织相比,肺癌组织中PTTG1和MMP9的mRNA和蛋白质表达水平显著上调。在人支气管上皮BEAS-2B细胞系中诱导了PTTG1或MMP9的过表达,这表明单独增加PTTG1或MMP9不仅可能促进细胞迁移、增殖并诱导集落形成,还可能抑制细胞凋亡。总之,PTTG1和MMP9被确定为通过基因治疗对肺癌进行治疗干预的潜在靶点。