Background Uridine cytidine kinase 2 (UCK2) is overexpressed in multiple tumors, whereas there are few studies on the regulation mechanism of UCK2 in lung adenocarcinoma.
Objective To study the effect of UCK2 on growth of LUAD and explore its possible mechanism.
Methods Using the RNA-seq data of LUAD in TCGA database, we screened differential genes by univariate independent prognostic analysis. Combined with clinical data, the genes related to the stage and prognosis of lung adenocarcinoma were screened. The cell proliferation and migration ability were detected by CCK-8 and wound healing test. The mechanism of UCK2 on the growth regulation of lung adenocarcinoma was analyzed by GSEA. Western blot was performed to explore the regulatory effect of the target gene on mTOR pathway in lung adenocarcinoma cells. The effects of UCK2 on glycolysis of lung adenocarcinoma cells through mTOR pathway were measured by glucose uptake, lactic acid and ATP.
Results Among the lung adenocarcinoma patients in the TCGA database, UCK2 was positively correlated with the stage of lung adenocarcinoma and negatively correlated with clinical prognosis. Compared with the NC group, overexpression of UCK2 promoted the growth and migration of A549 and Calu3 cells (P＜0.001). The high expression of UCK2 was positively correlated with the activation of mTOR pathway in LUAD identified by GSEA. Western blot analysis indicated that protein relative expression levels of p-PI3K, p-AKT, p-mTOR significantly increased by UCK2 in A549 cells (P＜0.001). UCK2 increased glucose uptake, lactate and ATP in A549 cells by regulating mTOR pathway.
Conclusion UCK2 promotes the growth and migration of lung adenocarcinoma by activating mTOR pathway.
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