NUP37 silencing induces inhibition of cell proliferation, G1 phase cell cycle arrest and apoptosis in non-small cell lung cancer cells.

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 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.

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