Search

Abstract Background Observational studies and experimental evidence have shown that chemokines play important roles in lung cancer development, progression, and treatment. However, few studies have examined the causal association between them. Methods Summary data of chemokines and lung cancer were obtained from genome-wide association studies. Mendelian randomization (MR) analyses were performed by five methods, Inverse variance weighted (IVW), Weighted median estimation, MR-Egger, Simple mode and Weighted, with IVW as the primary analysis method. Sensitivity analysis was used to assess the reliability of the MR results. Multivariate Mendelian randomization studies were used to infer whether causality was influenced by potential mediators. The expression levels of CCL21 were analyzed by quantitative real-time PCR. Results We found that CCL21 was negatively associated with lung adenocarcinoma risk. CCL25 was positively associated with lung squamous cell carcinoma risk. CCL5 was negatively associated with small cell lung cancer risk. CCL21, CCL24, CCL27, and CCL28 was positively associated with small cell lung cancer risk. After multivariate Mendelian randomization adjustment for smoking behavior, it was found that the effect of CCL25 on lung squamous cell cancer disappeared, and the effect of CCL21 on small cell lung cancer was quite opposite to the univariate. The receiver operating characteristic curve indicated that chemokines had high accuracy in the diagnosis of lung cancer. CCL21 expression levels showed large differences in lung adenocarcinoma cells. Conclusion These results highlighted the causal effects of chemokines on lung cancer and suggested a mediating role of smoking behavior in the association between chemokines and lung cancer.

Abstract Background Surgical approach in the treatment of thymoma is varied. This retrospective study aimed to evaluate the outcomes of different surgical approaches in the treatment of thymoma. Methods From January 2020 to December 2023, a total of 208 patients underwent thoracoscopic surgical treatment and were diagnosed with thymoma by postoperative pathological result in our institution. We collected and then analysed potential factors including general conditions, surgical approaches, preoperative clinical symptoms, surgical procedures, postoperative hospital stay, postoperative drainge, postoperative pain score, postoperative complications and postoperative follow-up. Results Of the 208 patients, 98 patients underwent surgery via subxiphoid approach (47.1%) and 110 patients via lateral intercostal approach (52.8%). The duration of the surgical procedure (P = 0.02), intraoperative blood loss (P = 0.045), total postoperative drainage (P = 0.021), postoperative drainage per day (P = 0.004) and Postoperative pain score (Day1 P = 0.010 and Day2 P = 0.002)showed a significant difference between these two groups. 31 patients (14.9%) received postoperative radiotherapy. One patient died due to postoperative radiotherapy. No recurrence occurred in one-year follow-up. Conclusions The present study not only showed that subxiphoid approach was a safe and feasible technique for thymoma, with a potentially faster postoperative recovery and less postoperative pain.

Abstract Background Phospholipase C Delta 3 (PLCD3) is a member of phospholipase C(PLC) Protein and PLCD3 protein plays a prominent role in many cancers. However, little is known about the role of PLCD3 in esophageal squamous cell carcinoma (ESCC). Material and Methods We analyzed PLCD3 mRNA and protein expression in ESCC tissues and cell lines by immunohistochemistry, quantitative real-time PCR, and western blot. The correlation between PLCD3 expression and clinicopathological characteristics was also analyzed. CCK8, colony formation, wound-healing, and transwell assays were conducted to measure cell functional alternations. Flow cytometry was performed to assess the apoptosis rate and cell cycle caused by PLCD3 knockdown. Xenograft models in nude mice to clarify the role of PLCD3 in ESCC. Key proteins in the PI3K / AKT signaling pathway after treatment of ECA109 and KYSE150 cells with the AKT inhibitor MK2206 were analyzed by western blot. Results PLCD3 was highly expressed in ESCC tissues and cell lines. PLCD3 expression levels correlated with pathologic stage and lymphatic metastasis. PLCD3 knockdown inhibited cell proliferation, migration, invasion, promoted apoptosis, and caused the cell cycle arrest in the G1 phase. PLCD3 overexpression promoted cell proliferation, migration, and invasion. In vivo experiments with xenografts demonstrated that PLCD3 promoted ESCC tumorigenesis. Finally, Overexpression of PLCD3 activated the PI3K / AKT / P21 signaling. Conclusion PLCD3 promotes malignant cell behaviors in esophageal squamous cell carcinoma via the PI3K/AKT/P21 signaling and could serve as a potential target for ESCC treatment.

Abstract Objective To investigate the predictive merit of combined preoperative nutritional condition and systemic inflammation on the prognosis of patients receiving esophagectomy, with the assessment of model construction to extract a multidisciplinary phantom having clinical relevance and suitability. Methods The software of R 4.1.2 was utilized to acquire the survival optimal truncation value and the confusion matrix of survival for the continuity variables. SPSS Statistics 26 was employed to analyze the correlation of parameters, where including t-test, ANOVA and the nonparametric rank sum test shall. Pearson chi-square test was used for categorical variables. The survival curve was retrieved by Kaplan–Meier method. Univariate analysis of overall survival (OS) was performed through log-rank test. Cox analysis was for survival analyze. The performance of the prediction phantom through the area under curve (AUC) of receiver operating characteristic curve (ROC), decision curve analysis (DCA), nomogram and clinical impact curve (CIC) was plotted by R. Results The AUC value of albumin-globulin score and skeletal muscle index (CAS) is markedly superior. Patients with diminished AGS and greater SMI were associated with improved overall survival (OS) and recurrence-free survival (RFS) (P

Abstract Background Tripartite Motif Containing 11 (TRIM11), a member of TRIM proteins, is overexpressed in high-grade gliomas and plays an oncogenic function in glioma biology. However, little is known about the role of TRIM11 in lung cancer. Methods We analyzed TRIM11 mRNA expression in lung cancer tissues and adjacent non-neoplastic tissues by real-time PCR. We then explored the function of TRIM11 in lung cancer cells by small interfering RNA-mediated downregulation of this protein followed by analyses of cell proliferation, migration and invasion. Results TRIM11 was highly expressed in lung cancer tissues and lung cancer cell lines. The higher expression of TRIM11 was correlated with the poorer prognosis of patients. Suppressing of TRIM11 expression in lung cancer cells with higher expression of TRIM11 (A549 and NCI-H446 cells) significantly reduced cell growth, motility and invasiveness. We further demonstrated that knockdown of TRIM11 affected the expression of cell proliferation-related proteins (Cyclin D1 and PCNA), and epithelial-mesenchymal transformation-related proteins (VEGF, MMP-2, MMP-9, Twist1, Snail and E-cadherin). The activity of ERK and PI3K/AKT was also suppressed in TRIM11 knocked down cells. Further experiments in lung cells with lower expression of TRIM11 (NCI-H460 and NCI-H1975 cells) with AKT inhibitor suggested that TRIM11 may promote cell motility and invasiveness through AKT pathway. Conclusions Our results indicate that TRIM11 acts as an oncogene in lung cancer through promoting cell growth, migration and invasion. Our findings may have important implication for the detection and treatment of lung cancer.