The aim of this research is to determine the role of human asparagine synthetase (ASNS) in human lung cancer. In the present study, immunohistochemical staining and the Oncomine database mining showed that the expression of ASNS gene was higher in lung cancer tissues than that in the normal tissues by. In addition, western blot assay showed that ASNS was elevated in lung cancer A549 and 95D cell lines as compared with that in H1299 and H460 cells. Therefore, A549 and 95D cells were chosen for subsequent MTT and colony formation assay. It was found that knockdown of ASNS inhibited the growth and colony formation abilities of A549 and 95D cells. Flow cytometry showed that ASNS silencing arrested cell cycle progression at G0/G1 phase in A549 cells, probably through regulating the expression of cell cycle molecules such as CDK2 and Cyclin E1 as shown by quantitative real-time PCR. Taken together, our study indicates that ASNS may be an important target for lung cancer diagnosis and treatment.

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Purpose: Lamina-associated polypeptide 2 (LAP2; encoded by TMPO ), is a nuclear protein that may affect chromatin regulation and gene expression through dynamically binding to nuclear lamin. TMPO (LAP2) plays dual roles of either suppressing or promoting proliferation of cells, depending on the status of the cell. It has been reported that TMPO is up-regulated in various cancer types. However, its function in lung cancer has not been studied yet. Materials and methods: A series of clinical microarray datasets for lung cancer were investigated to demonstrate the expression of TMPO. The transcription of TMPO gene in human lung cancer was analyzed using Oncomine platform (www.oncomine.org) according to the standardized procedures described previously. Four separate datasets (Hou Lung, Okayama Lung, Beer Lung, and Garber Lung) were analyzed. Results: Here, we show that TMPO is over-expressed in lung cancer tissues, and that a high level of TMPO indicates a poor prognosis in lung cancer patients. Knockdown of TMPO in lung cancer cells inhibits cell proliferation and induces apoptosis. Also, down-regulation of TMPO leads to an impaired metastatic ability of tumor cells. A nude mice tumor model show that knockdown of TMPO suppresses tumor formation in vivo. Conclusion: Collectively, this study suggests TMPO as an oncogene and a novel prognostic gene in lung cancer.