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BackgroundUsnic acid (UA), a secondary metabolite, is mainly derived from certain lichen species. Growing evidence suggests that UA has antitumor, anti-oxidative, anti-inflammatory, and other activities in a variety of cancer cells. However, the antitumor effect of UA in gastric cancer cells (GC) is unclear. The aim of this investigation was to assess the antitumor effect of UA in GC cells in vitro and in vivo, and to explore the underlying mechanisms.Material/MethodsCell proliferation was measured by CCK8 assay, the arrest of cell cycle was assessed by flow cytometry, and cellular apoptosis was observed via Hoechst 33258 staining assay. Expression levels of apoptosis-related proteins (activated caspase-3 and PARP, Bax, Bcl2) and autophagy-associated proteins (LC3-II and p62) were verified through Western blot analysis. H&E staining and immunohistochemistry were carried out in the subcutaneously implanted BGC823 tumor model in a nude mouse experiment.ResultsIn vitro, we demonstrated that UA was significantly effective in inducing morphological changes, inhibiting the cell proliferation dose- and time-dependently, arresting the cell cycle phase, promoting cancer cellular apoptosis, and inducing autophagy activity. In vivo, compared to mice treated with 5-FU alone, UA treatment was significantly more effective in suppressing the tumor growth without affecting body weight, and in regulating the amount of Bax and Bcl2 in tumor tissues.ConclusionsUA induces cell cycle arrest and autophagy and exerts anti-proliferative and apoptotic effects by modulating expression of apoptosis-related proteins in stomach neoplasm cells, and has a better antitumor effect compared to 5-Fu in the xenograft model.

The aim of the present study was to investigate the effect of cantharidin (CTD) on human gastric cancer cells and to explore the underlying mechanisms of these effects. The human gastric cancer SGC-7901 and BGC-823 cell lines were treated with CTD. MTS assays were then employed to examine cellular proliferation, flow cytometry was used to analyze the cell cycle and apoptosis, and western blot analysis was used to determine protein expression levels. It was found that CTD inhibited the proliferation of the human gastric cancer SGC-7901 and BGC-823 cells in a dose- and time-dependent manner in vitro. CTD also induced G2/M phase arrest and cellular apoptosis in a dose-dependent manner. In addition, CTD increased the levels of p21, caspase-7, -8 and -9, activated caspase-3, poly ADP ribose polymerase and Bad, but decreased the levels of cyclin-dependent kinase 1, cyclin A and B, B-cell lymphoma-2 (Bcl-2) and Bid. The present results suggested that CTD may inhibit the proliferation of human gastric cancer SGC-7901 and BGC-823 cells in vitro by inducing G2/M phase arrest and cell apoptosis. CTD may induce cellular G2/M phase arrest by regulating cycle-associated proteins and induce apoptosis by activating a caspase cascade or regulating the Bcl-2 family proteins.

BackgroundTo perform a meta-analysis evaluating the diagnostic ability of fecal lactoferrin (FL) to distinguish inflammatory bowel disease (IBD) from irritable bowel syndrome (IBS).MethodsThe Medline, EMBASE, Web of Science, Cochrane library and CNKI databases were systematically searched for studies that used FL concentrations to distinguish between IBD and IBS. The sensitivity, specificity, and other diagnostic indexes of FL were pooled using a random-effects model.ResultsSeven studies, involving 1012 patients, were eligible for inclusion. In distinguishing IBD from IBS, FL had a pooled sensitivity of 0.78 (95% confidence interval [CI]: 0.75, 0.82), a specificity of 0.94 (95% CI: 0.91, 0.96), a positive likelihood ratio of 12.31 (95% CI: 5.93, 29.15), and a negative likelihood ratio of 0.23 (95% CI: 0.18, 0.29). The area under the summary receiver-operating characteristic curve was 0.94 (95% CI: 0.90, 0.98) and the diagnostic odds ratio was 52.65 (95% CI: 25.69, 107.91).ConclusionsFL, as a noninvasive and simple marker, is useful in differentiating between IBD and IBS.

BackgroundMetabolic syndrome (MetS) is associated with carotid intima-media thickness (CIMT), which is a good predictor of cardiovascular disease (CVD). However, among individuals with MetS, direct comparative data regarding the utility of the apoB/apoAΙ ratio and the non-HDL-C/HDL-C ratio to diagnose carotid atherosclerosis are scarce, particularly in Chinese populations. We aimed to determine the relationship between the apoB/apoAΙ ratio and the non-HDL-C/HDL-C ratio and carotid atherosclerosis among Chinese individuals with MetS.MethodsWe performed a retrospective study of 5822 Chinese participants who underwent a routine health screening examination. Lipid profiles, fasting glucose, fasting insulin, CRP, apoB, apoAΙ and CIMT were measured.ResultsWe observed that among Chinese individuals with MetS, men (53.95 ± 0.58 ys) developed carotid atherosclerosis at a younger age than women (58.47 ± 1.17 ys) (P < 0.001). Both the apoB/apoAΙ ratio and the non-HDL-C/HDL-C ratio positively correlated with carotid atherosclerosis among Chinese individuals with MetS, particularly among women. Meanwhile, CIMT increased progressively across the quartiles of the non-HDL-C/HDL-C ratio (P for trend, < 0.05). Receiver Operating Characteristic (ROC) analysis indicated that the AUC of the apoB/apoAΙ ratio (0.561) was higher than that of the non-HDL-C/HDL-C ratio (0.522) in men (P < 0.05) and the AUC of the apoB/apoAΙ ratio (0.640) was lower than that of the non-HDL-C/HDL-C ratio (0.695) in women (P < 0.05). Among Chinese individuals with MetS, the AUC of the non-HDL-C/HDL-C ratio was more prominent among women compared with men (P < 0.05).ConclusionOur findings indicate that among individuals with MetS, Chinese men develop carotid atherosclerosis at a much younger age than women. There were no significant differences between the apoB/apoAΙ ratio and the non-HDL-C/HDL-C ratio for the prediction of carotid atherosclerosis among Chinese individuals with MetS. Among Chinese individuals with MetS, the utility of the non-HDL-C/HDL-C ratio was found to be greater among women than among men.

Background Helicobacter pylori is an important carcinogenic factor in gastric cancer. Studies have shown that Helicobacter pylori infection is inversely associated with certain diseases such as esophageal cancer and whose infection appears to have a “protective effect.” At present, the relationship between Helicobacter pylori infection and esophageal cancer remains controversial. This study was designed to investigate the relationship between Helicobacter pylori infection and the risk of esophageal cancer in different regions and ethnicities. Methods Systematic search of the articles on the relationship between Helicobacter pylori infection and esophageal cancer from the database with the duration time up to December 2018. This systematic review was performed under the MOOSE guidelines. Results This meta-analysis included 35 studies with 345,886 patients enrolled. There was no significant correlation between Helicobacter pylori infection and esophageal squamous cell carcinoma in the general population (OR: 0.84; 95% CI: 0.64-1.09/OR: 0.74; 95% CI: 0.54-0.97). However, a significant correlation was found in the Middle East (OR: 0.34; 95% CI: 0.22-0.52/95% CI: 0.26-0.44). There was no significant difference in the prevalence of Helicobacter pylori between the case group and the control group in esophageal adenocarcinoma (8.87% vs. 9.67%). The pooled OR was 0.55 (95% CI: 0.43-0.70) or 0.23 (95% CI: 0.15-0.36). When grouped by match or not, the pooled OR of the nonmatching group and the matching group was 0.48/0.21 (95% CI: 0.36-0.65/95% CI: 0.13-0.36) and 0.73/0.71 (95% CI: 0.57-0.92/95% CI: 0.60-0.84), respectively. Conclusion In the general populations, no significant association was found between Helicobacter pylori infection and the risk of esophageal squamous cell carcinoma. However, lower risk was found in the Middle East. Helicobacter pylori infection may reduce the risk of esophageal adenocarcinoma, but such “protection effect” may be overestimated.

Aims: To profile and characterize the circular RNA (circRNA) expression pattern in poorly differentiated gastric adenocarcinoma (PDGA). Methods & materials: CircRNA expression profiles in PDGA and adjacent nontumor tissues were analyzed by microarray. Five randomly selected differentiated expressed circRNAs (DECs) were validated by real-time quantitative PCR. m6A qualification of the top 20 DECs was conducted by m6A-immunoprecipitation and real-time quantitative PCR. Results: A total of 65 DECs were found in PDGA compared with the control. Hsa_circRNA_0077837 had the largest area under the curve. Most DECs had m6A modifications, the trend of m6A modification alteration was mainly consistent with the circRNA expression level. Conclusion: Our study revealed a set of DECs and their m6A modification alterations, which may provide new insight for their potential function in PDGA.