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Abstract Background Calcium-activated nucleotidase 1 (CANT1), functions as a calcium-dependent nucleotidase with a preference for UDP. However, the potential clinical value of CANT1 in lung adenocarcinoma (LA) has not been fully clarified. Thus, we sought to identify its potential biological function and mechanism through bioinformatics analysis and in vitro experiments in LA. Methods In the present study, we comprehensively investigated the prognostic role of CANT1 in LA patients through bioinformatics analysis and in vitro experiments. The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) were utilized to analyze the expression of CANT1 in LA patients and their clinical-prognostic value. The immunohistochemistry staining was obtained from the Human Protein Atlas (HPA). A Cox regression model was used to evaluate prognostic factors. Gene ontology (GO) and Gene set enrichment analysis (GSEA) was performed to explore the potential regulatory mechanism of CANT1 in the development of LA. Moreover, we also examined the relationship between CANT1 expression and DNA methylation. Finally, we did in vitro experiments to evaluate the biological behavior and role of CANT1 in LA cells (LACs). Results Our study showed that the CANT1 expression was significantly elevated in the LA tissues compared with the normal lung tissues. Increased CANT1 expression was significantly associated with the TN stage. A univariate Cox analysis indicated that high CANT1 expression levels were correlated with poor overall survival (OS) in LA. Besides, CANT1 expression was independently associated with OS in multivariate analysis. GO and GSEA analysis showed the enrichment of mitotic nuclear division, DNA methylation, and DNA damage. Then we found that the high expression of CANT1 is positively correlated with hypomethylation. The methylation level was associated with prognosis in LA patients. Finally, in vitro experiments indicated that knockdown of CANT1 resulted in decreased cell proliferation, invasion, and G1 phase cell-cycle arrest in LACs. Conclusion The present study suggested that CANT1 may serve as a potential prognosis biomarker in patients with LA. High CANT1 expression and promoter demethylation was associated with worse outcome. Finally, in vitro experiments verified the biological functions and behaviors of CANT1 in LA.

Abstract Objective There is still no definitely therapeutic evidence of a beneficial effect of chemotherapy with radiotherapy for older patients with esophageal squamous cell carcinoma (ESCC). We aim to determine the influence of chemoradiotherapy (CRT) and radiotherapy (RT) alone in patients aged 65 years or older with locally advanced ESCC. Methods We retrospectively analyzed 581 ESCC patients who underwent CRT and RT alone. Univariate and multivariate Cox regression analysis was used to analyze the impact of clinical factors on long‐term overall survival (OS) and progression-free survival (PFS). Finally, we compared the toxicity rates of these patients. Results The median OS and PFS of the overall population were 23.2 months (2.0–162.6 months) and 18.6 months (1.1–159.6 months). Multivariate Cox regression analysis showed that chemotherapy (p 0.05). Besides, higher staged ESCC has the inferior OS and PFS than lower staged ESCC for patients received RT alone and aged 65–74 years (both p

Abstract Background Lung cancer is the most common malignant tumor. Identification of novel diagnostic and prognostic biomarkers for lung cancer is a key research imperative. The role of centromere protein K (CENPK) in cancer is an emerging research hotspot. However, the role of CENPK in the progression of lung adenocarcinoma (LAC) is not well characterized. Methods In this study, we identified CENPK as a potential new gene for lung cancer based on bioinformatics analysis. In addition, in vitro experiments were performed to verify the function of this gene. We investigated the expression of CENPK in LAC by analyses of datasets from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Differential expression analyses, gene ontology (GO) enrichment, Kyoto encyclopedia of genes and genomes (KEGG) analysis, and gene set enrichment analysis (GSEA) were conducted to evaluate the diagnostic and prognostic relevance of CENPK. Then, for evaluating the biological behavior and role of CENPK in lung cancer cells, we did a series of vitro experiments, such as immunohistochemistry analysis, Western blot analysis, CCK8 assay, transwell assay, flow cytometry, and wound healing assay. Results We demonstrated overexpression of CENPK in LAC; in addition, increased expression of CENPK was associated with clinical progression. Moreover, CENPK was found to be an independent risk factor in patients with LAC. Furthermore, we observed activation of CENPK-related signaling pathways in patients with LAC. Conclusions Our findings indicate a potential role of CENPK in promoting tumor proliferation, invasion, and metastasis. It may serve as a novel diagnostic and prognostic biomarker in patients with LAC.