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Lung cancer has a complex etiology involving multiple regulatory systems. Uncertainty about the biology and evolution of lung cancer has made it difficult to improve its poor prognosis. To create efficient therapeutic targets and optimal molecular screening tools for lung cancer, the most important task seems to be to understand how it develops and progresses. The expression and regulation of GTPBP4 in non-small cell lung cancer (NSCLC) are not well understood. Using methods such as knocking down GTPBP4 in lung cancer cells and establishing a mouse lung cancer model, we found that the expression of GTPBP4 was upregulated in human lung adenocarcinoma cells and tissues, and that knocking down the expression of the GTPBP4 gene in A549 and Calu-1 lung adenocarcinoma cells can inhibit the proliferation of lung adenocarcinoma cells and reduce their invasion ability. The results of the mouse lung cancer model showed that the lung weight and the number of lung surface nodules decreased significantly in the LLC-GTPBP4 KO group. The mechanism by which GTPBP4 regulation affects the progression of lung adenocarcinoma may be related to the regulation of EMT. From this study, new research ideas emerge to explore GTPBP4 as a biomarker and therapeutic target for early diagnosis and treatment of lung cancer.

Treatment of cancer in humans requires a thorough understanding of the multiple pathways by which it develops. Recent studies suggest that nuclear receptor coactivator 4 (NCOA4) may be a predictive biomarker for renal cancer. In the present work, TCGA, GEPIA, and several bioinformatics approaches were used to analyze the NCOA4 expression patterns, prognostic relevance, and association between NCOA4 and clinicopathological features and immune cell infiltration. We investigated NCOA4 expression in malignancies. Low NCOA4 expression was associated with poor overall survival in individuals with malignancies such as cholangiocarcinoma, colon adenocarcinoma, and clear cell renal carcinoma. We also analyzed NCOA4 DNA methylation in normal and primary tumor tissues and investigated possible functional pathways underlying NCOA4-mediated oncogenesis. In conclusion, downregulation of NCOA4 is associated with poor prognosis, and NCOA4 may be a predictive biomarker for COAD.