ABSTRACT
Objective: To explore the risk factors of recurrence within 1 year after radical resection of non-small cell lung cancer (NSCLC) and construct the nomogram model. Methods: The clinical data of 186 patients with NSCLC treated with radical surgery in Affiliated Hospital of Youjiang Medical University for Nationalities of Baise were retrospectively analyzed. Multivariate logistic regression was applied to analyze the risk factors of recurrence within 1 year after radical resection of NSCLC. The R language (R 4.0.3 software package) was used in constructing the nomogram model, and the predictive value of the model was evaluated. Results: The recurrence rate of 186 patients within 1 year after radical surgery was 29.57%. After multivariate logistic regression analysis, pathological stage, number of lymph node metastasis, chronic obstructive pulmonary disease (COPD), postoperative plasma D-dimer, and carcinoembryonic antigen were independent factors for recurrence within 1 year after radical resection of NSCLC (P < 0.05). Based on the above independent risk factors, a nomogram model was established, with the distinction of AUC = 0.891 (95% CI: 0.819-0.964) and sensitivity and specificity of 70.3% and 97.8%, respectively. The calibration curve was close to the ideal curve. External validation of the model showed AUC = 0.801 (95% CI: 0.674-0.928), and sensitivity and specificity were 66.7% and 84.2%, respectively. Conclusion: The recurrence of NSCLC within 1 year after radical surgery was related to a variety of factors, and the nomogram model constructed based on risk factors had good goodness of fit, calibration, consistency of prediction, and prediction efficiency.
ABSTRACT
UCHL3 (Ubiquitin carboxyl-terminal hydrolase L3), a member of deubiquitinating enzymes, has been implicated in various cancers. However, the role of UCHL3 in esophageal squamous cell carcinoma (ESCC) remains unknown. In the current study, we aimed to investigate the role of UCHL3 in ESCC growth and migration, and whether UCHL3 could modulate CRY2 methylation through FOXM1. The expression of UCHL3 and CRY2 in ESCC tissues was assessed using qRT-PCR, western blotting and immunohistochemistry (IHC). Cell viability was determined by CCK-8 and colony formation assays. Hoechst 33342 and flow cytometry were used to detect cell apoptosis. Transwell assay was performed to investigate cell migration and invasion. In vivo animal model was used to assess cell tumorigenesis. Methylation-Specific PCR (MSP) was applied to detect CRY2 methylation in the promoter region. The results showed that UCHL3 expression was elevated in ESCC tissues and cells, while CRY2 expression was decreased. UCHL3 silencing inhibited cell viability, invasion, migration and induced cell apoptosis in vitro, repressed tumor growth in vivo, and increased CRY2 expression and decreased FOXM1 expression. In addition, UCHL3 knockdown decreased CRY2 methylation through downregulating FOXM1, leading to an increase in the expression of CRY2. Moreover, CRY2 silencing abolished UCHL3 deficiency-mediated inhibition in cell growth and migration. In summary, this study reveals that knockdown of UCHL3 inhibits ESCC growth and migration by reducing CRY2 methylation through downregulation of FOXM1 expression.
