AIM: To investigate the expression of forkhead box protein M1 (FoxM1) in the process of epithelial mesenchymal transition in hepatocellular carcinoma (HCC) and its role in metastasis. METHODS: FoxM1 and E-cadherin expression in HCC tissue microarray specimens was evaluated by immunohistochemical staining, and statistical methods were applied to analyze the correlation between FoxM1 and epithelial-mesenchymal transition (EMT). Kaplan-Meier analysis of the correlation between the FoxM1 expression level and recurrence or overall survival of HCC patients was performed. The expression of FoxM1, E-cadherin and snail homologue 1 (SNAI1) in HCC cell lines was evaluated by real-time reverse transcription-polymerase chain reaction and Western blot. Hepatocyte growth factor (HGF) was used to induce EMT and stimulate cell migration in HCC cells. The expression of FoxM1 and SNAI1 was regulated by transfection with plasmids pcDNA3.1 and siRNAs in vitro. The occurrence of EMT was evaluated by Transwell assay, morphologic analysis and detection of the expression of EMT markers (E-cadherin and vimentin). Luciferase and chromatin immunoprecipitation assays were used to evaluate whether SNAI1 is a direct transcriptional target of FoxM1. RESULTS: FoxM1 expression was increased significantly in HCC compared with para-carcinoma (10.7 ± 0.9 vs 8.2 ± 0.7, P < 0.05) and normal hepatic (10.7 ± 0.9 vs 2.7 ± 0.4, P < 0.05) tissues. Overexpression of FoxM1 was correlated with HCC tumor size, tumor number, macrovascular invasion and higher TNM stage, but was negatively correlated with E-cadherin expression in microarray specimens and in cell lines. FoxM1 overexpression was correlated significantly with HCC metastasis and EMT. In vitro, we found that FoxM1 plays a key role in HGF-induced EMT, and overexpression of FoxM1 could suppress E-cadherin expression and induce EMT changes, which were associated with increased HCC cell invasiveness. Next, we confirmed that FOXM1 directly binds to and activates the SNAI1 promoter, and we identified SNAI1 as a direct transcriptional target of FOXM1. Moreover, inhibiting the expression of SNAI1 significantly inhibited FoxM1-mediated EMT. CONCLUSION: FoxM1 overexpression promotes EMT and metastasis of HCC, and SNAI1 plays a critical role in FoxM1-mediated EMT.

Minimally invasive esophagectomy (MIE) was shown to be effective in reducing the morbidity and was adopted increasingly. The robot-assisted minimally invasive esophagectomy (RAMIE) remains in the initial stage of application. This study evaluated its safety and feasibility by comparing short-term outcomes of RAMIE and video-assisted minimally invasive esophagectomy (VAMIE). Between March 2016 and December 2017, 115 consecutive patients underwent RAMIE or VAMIE at our institute. The baseline characteristics, pathological data and short-term outcomes of these two group patients were collected and compared. RAMIE patients were propensity score matched with VAMIE patients for a more accurate comparison. Matching based on propensity scores produced 27 patients in each group. After propensity score matching (PSM), the baseline characteristics between the two groups were comparable. The operation time in RAMIE group was significantly longer than that in VAMIE group (349 and 294 min, respectively; P < 0.001). The blood loss volume in RAMIE group was less than that in VAMIE group (119 and 158 ml, respectively), but with no statistically significant difference (P = 0.062). There was no significant difference between the two groups with respect to the mean number of dissected lymph nodes (20 and 19, respectively; P = 0.420), postoperative hospital stay (13.8 and 12.7 days, respectively; P = 0.548), the rate of overall complications (37.0 and 33.3%, respectively; P = 0.776) and the rates of detailed complications between the two groups. The short-term outcomes of RAMIE is comparable to VAMIE, demonstrating safety and feasibility of RAMIE.

Non-small cell lung cancer (NSCLC) is the most common cancer and cause of cancer-related mortality globally. Increasing evidence suggested that the long non-coding RNAs (lncRNAs) were involved in cancer-related death. To explore the possible prognostic lncRNA biomarkers for NSCLC patients, in the present study, we conducted a comprehensive lncRNA profiling analysis based on 1902 patients from Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) datasets. In the discovery phase, we employed 682 patients from the combination of four GEO datasets (GSE30219, GSE31546, GSE33745 and GSE50081) and conducted a seven-lncRNA formula to predict overall survival (OS). Next, we validated our risk-score formula in two independent datasets, TCGA (n=994) and GSE31210 (n=226). Stratified analysis revealed that the seven-lncRNA signature was significantly associated with OS in stage I patients from both discovery and validation groups (all P<0.001). Additionally, the prognostic value of the seven-lncRNA signature was also found to be favorable in patients carrying wild-type KRAS or EGFR. Bioinformatical analysis suggested that the seven-lncRNA signature affected patients' prognosis by influencing cell cycle-related pathways. In summary, our findings revealed a seven-lncRNA signature that predicted OS of NSCLC patients, especially in those with early tumor stage and carrying wild-type KRAS or EGFR.