Breast cancer is one of the most prevalent malignancies and the leading cause of cancer-associated mortality in women worldwide and in China. Everolimus (C53H83NO14) is an efficient anti-cancer drug for breast cancer which targets mammalian target of rapamycin (mTOR). The present study investigated the inhibitory effects of everolimus on breast cancer cells and an MCF-7-bearing mouse model. The potential mechanism of the everolimus-mediated decrease in growth and aggressiveness of breast cancer cells was reported. Results demonstrated that everolimus significantly inhibited breast cancer cell growth, migration and invasion. It was demonstrated that everolimus induced apoptosis through decreasing B cell lymphoma (Bcl)-2 and Bcl-w and increasing caspase-3 and caspase-8 expression levels in breast cancer cells. It was observed that everolimus decreased phosphoinositide 3-kinase (PI3K), protein kinase B (AKT) and mTOR expression levels in breast cancer cells. Results additionally demonstrated that PI3 K overexpression prevented that everolimus-mediated inhibition of growth and aggressiveness in MCF-7 cells. In vivo assays demonstrated that everolimus treatment markedly inhibited tumor growth in the MCF-7 bearing mouse model. Overall, these data indicate that everolimus inhibits growth and aggressiveness of breast cancer cells through the PI3K/AKT/mTOR signaling pathways, suggesting the PI3K/AKT/mTOR signaling pathway may act as a therapeutic target for the treatment of human cancer.

This study aimed to identify potential biomarkers and the therapeutic targets for colorectal adenocarcinoma by systematically evaluate a large scale of long noncoding RNAs (lncRNAs) expression data from TCGA. The algorithm t-distributed stochastic neighbor embedding and hierarchical clustering were utilized to group the samples into three clusters that showed a different prognosis. To identify the relationship between the clustered groups and different histoclinical features, different statistical methods were used. The functions of LINC01234 and MIR210HG were investigated with the help of the public database. The results showed that the expression levels of lncRNAs were able to distinguish the tumor samples from the normal tissues and in further they were able to predict the prognosis of the patients. We proposed two potential lncRNAs, which might serve as a biomarker or therapeutic targets. LINC01234 can be a good biomarker. In contrast, MIR210HG participated in the progression of colorectal adenocarcinoma by regulating hypoxia. It might function through an lncRNA-microRNA-messenger RNA regulatory network with MIR210 and RASSF7. K E Y W O R D S colorectal adenocarcinoma, LINC01234, long noncoding RNAs (lncRNAs), MIR210HG, survival analysis

BackgroundThe beneficial effect of surgical resection for hepatic metastasis from gastric cancer (HMGC) remains elusive. This study was conducted to analyze surgical outcomes of HMGC and determine the prognostic factors associated with survival.ResultsThe in-hospital mortality rate was zero, and the overall morbidity rate was 56%. The overall 1-, 3-, and 5-year survival rate after surgery was 87.5%, 47.6%, and 21.7%, respectively, with a median survival time of 34.0 months. Multiple liver metastases (hazard ratio [HR] =1.998; 95% confidence interval [CI] = 1.248-3.198; P = 0.004) and ≥ T3 stage of the primary gastric cancer (HR = 2.065; 95% CI = 1.201–3.549; P = 0.009) were independent prognostic determinants in the multivariate analysis.Materials and MethodsData on surgical resection of 96 patients with HMGC at six institutions in China were analysed retrospectively. Prognostic factors were assessed by multiple stepwise regression analysis using the Cox model.ConclusionsSurgical resection for HMGC is feasible and beneficial to long-term survival in selected patients.

Background: We carried out a meta-analysis to determine the effectiveness of breast conservation therapy (BCT) or mastectomy (MT) for stage I or stage II breast cancer.Methods: A fully recursive literature search was conducted in the Cochrane Controlled Trials Register Databases, Medline, EMBASE and Chinese Biomedical Literature Database in any language. Randomized controlled trials (RCTs) were considered for inclusion. Analyses were carried out using RevMan software.Results: In all, 18 RCTs including a total of 9388 patients were included. The meta-analysis showed that the overall survival in 3, 5, 10, 15 and 20 years and the locoregional recurrence rate in 3, 5, 15 and 20 years were not statistically significantly different between group BCT and group MT, but 10-year locoregional recurrence rate increased in group BCT. The sensitivity analysis indicated that both overall survival and locoregional recurrence rate were not statistically significant difference between group BCT and group MT. In the subgroup analysis, there was no significant difference in OS and locoregional recurrence rate between group BCT and group MT, but 20-year locoregional recurrence rate was statistically significantly higher in group BCT than group MT for women with tumors 2 cm or smaller.Conclusion: BCT was better choice than MT for women with stage I or stage II breast cancer.

Recently, increasing evidence has indicated lncRNAs are powerful regulators in the progression of multiple tumors. Dysregulation of lncRNA NEAT1 has been recognized in many cancer types. Meanwhile, the studies on NEAT1 function have suggested that NEAT1 can serve as a crucial oncogene. Nevertheless, the investigation of NEAT1 in colon cancer is still few. In our study, the function of NEAT1 was studied in colon cancer. As we observed, NEAT1 level was obviously elevated in colon cancer cells.Then, HCT-116 and SW620 cells were stably infected with shRNA-NEAT1 for 48 hr.As exhibited, silence of NEAT1 could greatly repress colon cancer cell progression. Apoptosis of colon cancer cells was triggered and the cell cycle progression wasremarkably inhibited by downregulation of NEAT1. Interestingly, as exhibited, miR-495-3p was obviously decreased in colon cancer cells and it significantly suppressed colon cancer progression. Subsequently, miR-495-3p was predicted as a target of NEAT1. CDK6 was speculated as the target of miR-495-3p and miR-495-3p modulated its expression negatively. Finally, it was indicated that NEAT1 promoted colon cancer development through modulating miR-495-3p and CDK6 in vivo. Taken these together, we reported that NEAT1 could sponge miR-495-3p to contribute to colon cancer progression through activating CDK6. K E Y W O R D SCDK6, colon cancer, miR-495-3p, NEAT1