Abstract
Lung adenocarcinoma (LUAD) is the most prevalent histologic type of lung cancer, associated with a high incidence rate and substantial mortality rate worldwide. Accumulating evidence shows that the aberrant expression of neuromedin U (NMU) contributes to the initiation and progression of cancer. Herein, we explored whether NMU could be adopted as a new diagnostic and therapeutic marker in LUAD. The UALCAN and GEPIA web resources were employed to assess data on the NMU expression in LUAD. The STRING web resource was used to develop the PPI (protein-protein interaction) network of NMU, whereas Cytoscape was applied for module analysis. The Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of NMU and the interacting proteins were examined using the WebGestalt tool. Survival analysis was performed with the Kaplan-Meier plotter tool. Results revealed that the NMU expression in LUAD was significantly higher than in the nonmalignant tissues. Moreover, higher NMU levels were dramatically related to shorter overall survival, first progression survival, and postprogression survival. The specific gene mutations G45V, R143T, and F152L of NMU occurred in LUAD samples and were associated with a worse prognosis in patients. KEGG and western blot analyses demonstrated an association of NMU with the cell cycle and the cAMP signaling cascade. Bioinformatic analysis and the in vitro experiments implicated NMU as a promising prognostic signature and treatment target for LUAD.
Highlights
Lung cancer is among the malignant tumors associated with high incidence and mortality rates worldwide [1]
The association of the neuromedin U (NMU) expression levels with clinicopathological features of Lung adenocarcinoma (LUAD) patients was explored via the UALCAN data resource
The elevated NMU expression was related to the remarkable dismal OS, FPS, and PPS in LUAD patients, suggesting that NMU potentially plays an indispensable role in LUAD prognosis
Summary
Lung cancer is among the malignant tumors associated with high incidence and mortality rates worldwide [1]. Great advancements in the treatment of patients with lung adenocarcinoma have been made, including surgery, radiotherapy, chemotherapy, or targeted therapy [3]. Recent studies have revealed the potential of targeted therapy in the repression of the growth of lung cancer cells by inhibiting the activation of key oncogenic molecules which drive LUAD progression [4,5,6]. Targeted therapy yields promising results in early treatment, the development of drug resistance is linked to treatment failure [7]. There is a need to uncover critical genes and signaling cascades that mediate tumor progression of LUAD to develop advanced therapeutic strategies for LUAD management
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