Gastric cancer is the third leading cause of cancer-associated deaths worldwide. Research into the underlying mechanisms of gastric cancer is essential for the development of novel therapeutic agents to improve the prognoses of patients with gastric cancer. Tanshinone IIA (Tan IIA) is the pure extract of Danshen root (Salvia miltiorrhiza) and has been report to inhibit the proliferation of gastric cancer cells; however, the intrinsic underlying mechanisms remain unclear. The aim of the present study was to investigate whether Tan IIA has a direct anti-cancer effect in gastric cancer cells and determine the underlying mechanisms responsible. The results revealed that Tan IIA effectively inhibits proliferation in three human gastric cancer cell lines (SNU-638, MKN1 and AGS) in a time- and dose-dependent manner. Furthermore, Tan IIA treatment induced an increase in apoptosis, B-cell lymphoma (Bcl-2)-associated protein X expression and cleaved caspase-3 levels, as well as a decrease in Bcl-2 expression. Treatment with Tan IIA inhibited Furthermore, treatment with Tan IIA significantly inhibited the phosphorylation of signal transducer and activator of transcription 3 (STAT3), which may be responsible for the changes in apoptosis gene expression. However, overexpression of STAT3 significantly ameliorated the Tan IIA-induced suppression of cell growth and apoptosis. A nude mouse xenograft model was constructed and the results revealed that intraperitoneal Tan IIA treatment for 28 days significantly inhibited tumor growth and STAT3 activation. The results of the present study suggest that Tan IIA exerts potent anti-cancer activity in gastric cancer cells and this effect is mediated by the downregulation of STAT3 activation.

Background:Increasing evidence has supported the link of intestinal Fusobacterium nucleatum infection to colorectal cancer (CRC). However, the value of F. nucleatum as a biomarker in CRC detection has not been fully defined. In order to reduce the random error and bias of individual research, this meta-analysis aimed to evaluate the diagnostic performance of intestinal F. nucleatum in CRC patients and provide evidence-based data to clinical practice.Methods:An article search was performed from PubMed, Embase, Cochrane Library, and Web of Science databases up to December 2017, using the following key words: “Fusobacterium nucleatum”, ”Fusobacterium spp.”, ”Fn”, “colorectal cancer(s)”, “colorectal carcinoma(s)”, “colorectal neoplasm(s)”, and “colorectal tumor(s)”. Articles on relationships between F. nucleatum and CRC were selected according to the preestablished inclusion and exclusion criteria. This meta-analysis was performed using STATA 12.0 software, which included mapping of forest plots, heterogeneity tests, meta-regression, subgroup analysis, sensitivity analysis, and publication bias. The sensitivity, specificity, positive likelihood ratio (LR), negative LR, diagnostic odds ratio (DOR), and their corresponding 95% confidence interval (CI) of each eligible study were summarized.Results:Finally, data for 1198 participants (629 CRC and 569 healthy controls) in 10 controlled studies from seven articles were included. The summary receiver operator characteristic curve was mapped. The diagnostic performance of intestinal F. nucleatum infection on CRC was as follows: the area under the curve: 0.86 (95% CI: 0.83–0.89), the pooled sensitivity: 0.81 (95% CI: 0.64–0.91), specificity: 0.77 (95% CI: 0.59–0.89), and DOR: 14.00 (95% CI: 9.00–22.00).Conclusion:Intestinal F. nucleatum is a valuable marker for CRC diagnosis.

This study aims to investigate the mechanism by which biliary drainage reduces intestinal barrier damage in obstructive jaundice (OJ). A biliary drainage model was established in rats with OJ to detect changes in inflammatory factors and diamine oxidase (DAO), a marker of intestinal mucosal damage. The expression of autophagy-related genes in the intestinal mucosa after biliary drainage was detected using a reverse transcription-polymerase chain reaction. The rats were separated into two groups that received the autophagy activator rapamycin (RAPA) or the autophagy inhibitor 3-methyladenine (3-MA) to further investigate whether biliary drainage could alleviate the inflammatory response, oxidative stress, mitochondrial complex IV damage, and thus barrier damage in rats with OJ. The expression levels of inflammatory factors and the serum DAO content were increased in rats with OJ (P < 0.05). Biliary drainage further induced autophagy, reduced the expression levels of inflammatory factors, decreased the serum DAO content (P < 0.05), and improved intestinal mucosal damage. Administration of RAPA to OJ rats with biliary drainage increased autophagy (P < 0.05); decreased inflammatory factor secretion (P < 0.05), the serum DAO content (P < 0.05), oxidative stress (P < 0.05), and mitochondrial respiratory chain complex IV damage (P < 0.05); and ameliorated intestinal mucosal injury in OJ rats. When OJ rats were treated with 3-MA, intestinal mucosal injury, intestinal mitochondrial injury, and oxidative stress were all aggravated (P < 0.05). Biliary drainage can reduce the expression of inflammatory factors, oxidative stress, and mitochondrial injury by inducing intestinal mucosal autophagy in OJ rats, thus suggesting its role in the alleviation of intestinal mucosal injury.

The existing treatments have no satisfactory outcomes for hepatocellular carcinoma (HCC). LMO1 is abnormally expressed in several tumors, but its relationship with HCC is unclear. Therefore, we intend to evaluate LMO1’s role in HCC and the clinical significance. The HCC patients cancer tissues and adjacent tissues were collected. LMO1/control-siRNA was transfected into HepG2 cells followed by analysis of relevant protein expression by immunohistochemistry and Western blot, LMO1 mRNA level by qPCR, cell proliferation by CCK8 assay and apoptosis by flow cytometry. LMO1 positive rate was significantly elevated in HCC tissues relative to adjacent tissues. LMO1 expression was related to TNM stage and lymph node metastasis of tumor tissues (P <0.05). Patients with positive LMO1 level had a lower cumulative survival rate than those with negative expression (P <0.05). TNM stage, lymphatic metastasis and LMO1 expression were identified to be independent risk factors affecting HCC survival; cells transfected with LMO1-siRNA showed significantly reduced proliferation, increased cell apoptosis and upregulated bax as well as downregulated bcl-2 (P < 0.05). In conclusion, LMO1 may affect the occurrence and development of HCC through regulation of the bcl-2/bax expression.