Respiratory Medicine, Zhejiang Provincial Armed Police Corps Hospital, 304052, Jiaxing, Zhejiang, PR China.
Wenzhou Medical University, 325035, Wenzhou, Zhejiang, PR China.
Pathol Res Pract. 2020 Mar;216(3):152836. doi: 10.1016/j.prp.2020.152836. Epub 2020 Jan 21.
NUP37 has been reported as a component of the nuclear pore complex, which may be involved in tumorigenesis. Previous reports have shown that NUP37 acts as an oncogene in the development of hepatocellular carcinoma. However, its role in lung cancer remains unknown. The present study demonstrated for the first time that NUP37 expression was overexpressed in non-small cell lung cancer (NSCLC) samples compared with the corresponding expression noted in normal tissues. The results were derived by analyzing public datasets. Moreover, it was shown that NUP37 was overexpressed in advanced stage NSCLC samples compared with the corresponding expression of this protein in early stage NSCLC samples. Higher expression levels of NUP37 correlated with lower overall survival (OS) in NSCLC samples. Bioinformatic analysis indicated that NUP37 was involved in regulating cell cycle progression in NSCLC. Furthermore, knockdown of NUP37 suppressed cell growth and proliferation in A549and H1299 cells as demonstrated with the Celigo Cell Counting method and the MTT assay. Flow cytometry analysis indicated that knockdown of NUP37 induced significant S phage cell arrest and apoptosis in A549 and H1299 cells. The results showed that knockdown of NUP37 remarkably induced the protein levels of cleaved PARP, P53 and BCL2 in A549 cells. Therefore, it was concluded that NUP37 serves a distinguished role in the growth of lung cancer cells and may be considered as a potential biomarker and therapeutic target for lung cancer.
NUP37 已被报道为核孔复合物的一个组成部分，它可能参与肿瘤发生。先前的报告表明，NUP37 在肝细胞癌的发展中作为癌基因发挥作用。然而，其在肺癌中的作用尚不清楚。本研究首次表明，与相应的正常组织相比，NUP37 在非小细胞肺癌（NSCLC）样本中表达过度。这些结果是通过分析公共数据集得出的。此外，结果表明，与早期 NSCLC 样本中 NUP37 的表达相比，晚期 NSCLC 样本中 NUP37 表达过度。NUP37 表达水平较高与 NSCLC 样本的总生存期（OS）降低相关。生物信息学分析表明，NUP37 参与调节 NSCLC 中的细胞周期进程。此外，用 Celigo 细胞计数法和 MTT 检测法证实，敲低 NUP37 抑制了 A549 和 H1299 细胞的生长和增殖。流式细胞术分析表明，敲低 NUP37 可诱导 A549 和 H1299 细胞中 S 期细胞明显停滞和凋亡。结果表明，敲低 NUP37 可显著诱导 A549 细胞中 cleaved PARP、P53 和 BCL2 蛋白水平升高。因此，结论是 NUP37 在肺癌细胞的生长中起着显著的作用，并且可以被认为是肺癌的一个潜在的生物标志物和治疗靶点。
