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Gastric cancer (GC) is one of the most common tumors worldwide. Standard treatment after early detection involves surgical excision (recurrence is possible), and metastatic gastric cancer is refractory to immuno-, radio-, and most harmful chemotherapies. Various natural compounds have shown efficacy in killing different cancers, albeit not always specifically. In this study, we show that dandelion root extract (DRE) specifically and effectively suppresses proliferation and migration in human gastric cells without inducing toxicity in noncancerous cells. Long noncoding RNAs (lncRNAs) are known to promote tumorigenesis in many cancer types. Here, we showed that the lncRNA colon cancer-associated transcript-1 (CCAT1) was down-regulated in dandelion-treated GC cells. Furthermore, downregulation of CCAT1 inhibited proliferation and migration of gastric cells. We also found that DRE exerted its function in GC cells partially through targeting CCAT1. This data will provide a basis on which further research in cancer treatment through DRE can be executed.

A novel agarase-producing, non-endospore-forming marine bacterium, WH0801T, was isolated from a fresh seaweed sample collected from the coast of Weihai, China. Preliminary characterization based on 16S rRNA gene sequence analysis showed that WH0801Tshared 96.1 % similarity withAgarivorans albusMKT 106T, the type species of the genusAgarivorans. A polyphasic taxonomic study was conducted and confirmed the phylogenetic affiliation of strain WH0801Tto the genusAgarivorans. Isolate WH0801Tproduces light-yellow-pigmented colonies; cells are Gram-stain-negative, straight or curved rods, which are motile with a single polar flagellum. Strain WH0801Tgrew in 0.5–5 % NaCl, with optimum growth at 3 % NaCl, and its optimal pH and cultivation temperature were 8.4–8.6 and 28–32 °C, respectively. Data from biochemical tests, whole-cell fatty acid profiling, 16S rRNA gene sequence studies and DNA–DNA hybridization clearly indicated that isolate WH0801Trepresented a novel species within the genusAgarivorans, for which the nameAgarivorans gilvussp. nov. is proposed. The type strain ofAgarivorans gilvussp. nov. is WH0801T(=NRRL B-59247T=CGMCC 1.10131T).

Activated Leukocyte Cell Adhesion Molecules (ALCAM, also called CD166, MEMD) are cell surface immunoglobulins that are considered to be prognostic markers for breast cancer. CD166/ALCAM has gained increasing attention because of its significant association with tumor progression and the metastatic spread of breast cancer. Two polymorphisms have been identified in the CD166/ALCAM gene: 5'UTR C/T (rs6437585) and 3'UTR A/G (rs11559013). We analyzed the genotypes of 1033 individuals with breast cancer, and 1116 controls; odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using logistic regression. The effects and functions of polymorphisms were examined using luciferase gene expression assays and real-time PCR analyses. Our data demonstrated that individuals with the rs6437585 CT + TT genotype had an OR of 1.38 (95% CI, 1.11-1.72) for developing breast cancer, compared to those with the CC genotype. The T allele increased the risk of breast cancer in a dose-dependent manner (P (trend) < 0.001). However, there were no significant differences found between cases and controls at the rs11559013 A/G site. Additional experiments that we performed, which focused on reporter gene expression driven by CD166/ALCAM promoters, demonstrated that the presence of an rs6437585 T allele led to greater transcriptional activity than the rs6437585 C allele. This was consistent with the increased cancer risk that we observed in our case-control analysis.

The matrix metalloproteinases (MMP) can degrade various components of the extracellular matrix and its functional genetic polymorphisms may be associated with breast cancer risk. However, this relationship remains controversial. A meta-analysis was conducted in order to investigate the potential association between four polymorphisms in the MMP gene and breast cancer risk. A database search yielded a total of 9 studies involving 2,597 cases and 2,618 controls. Four polymorphisms were included in the meta-analysis: MMP-1 -1607 2G/1G (rs1799750), MMP-2 -1306 C/T (rs243865), MMP-3 -1171 6A/5A (rs3025058) and MMP-9 -1562 C/T (rs3918242). Crude odds ratios (OR) with 95% confidence intervals (CI) were used to assess the strength of association. When all the studies were pooled into the meta-analysis, we found that breast cancer cases had a significantly higher frequency of CC genotype (OR = 1.27, 95% CI = 1.10, 1.47; P = 0.001) and lower frequency of CT genotype (OR = 0.78, 95% CI = 0.67, 0.91; P = 0.001) of MMP-2. No significant difference was found in any genotype of MMP-1, MMP-3 or MMP-9. In conclusion, this meta-analysis suggested that MMP-2 -1306 C/T polymorphism may contribute to breast cancer susceptibility. More studies were needed especially in Asians in the future.

Half of the world's population experiences Helicobacter pylori (H. pylori) infection, which is a main cause of gastritis, duodenal and gastric ulcer, and gastric cancers. In the current study, we investigated the potential role of compound 13 (C13), a novel α1-selective small molecule activator of AMP-activated protein kinase (AMPK), against H. pylori-induced cytotoxicity in cultured gastric epithelial cells (GECs). We found that C13 induced significant AMPK activation, evidenced by phosphorylation of AMPKα1 and ACC (acetyl-CoA carboxylase), in both primary and transformed GECs. Treatment of C13 inhibited H. pylori-induced GEC apoptosis. AMPK activation was required for C13-mediated GEC protection. Inhibition of AMPK kinase activity by the AMPK inhibitor Compound C, or silencing AMPKα1 expression by targeted-shRNAs, alleviated C13-induced GEC protective activities against H. pylori. Significantly, C13 inhibited H. pylori-induced reactive oxygen species (ROS) production in GECs. C13 induced AMPK-dependent expression of anti-oxidant gene heme oxygenase (HO-1) in GECs. Zinc protoporphyrin (ZnPP) and tin protoporphyrin (SnPP), two HO-1 inhibitors, not only suppressed C13-mediated ROS scavenging activity, but also alleviated its activity in GECs against H. pylori. Together, these results indicate that C13 inhibits H. pylori-induced ROS production and GEC apoptosis through activating AMPK–HO–1 signaling. - Highlights: • We synthesized compound 13 (C13),more » a α1-selective small molecule AMPK activator. • C13-induced AMPK activation requires α1 subunit in gastric epithelial cells (GECs). • C13 enhances Helicobacter pylori-induced pro-survival AMPK activation to inhibit GEC apoptosis. • C13 inhibits H. pylori-induced reactive oxygen species (ROS) production in GECs. • AMPK-heme oxygenase (HO-1) activation is required for C13-mediated anti-oxidant activity.« less

Gastric cancer (GC) is one of the most common cancers worldwide, especially in Asia. The development of GC is a multifactorial process and numerous studies have linked genetic variation to GC risk. In this study, we evaluated the effects of single nucleotide polymorphisms (SNPs) of CD226 on GC susceptibility in Chinese populations including 687 cancer patients and 936 control subjects. We found that the G allele of the rs727088AG polymorphism in the 3'-untranslated region of CD226 was significantly associated with risk of GC using logistic regression (P10(-3)). GC patients who harbored the rs727088G allele had significantly increased cancer risk (odds ratio=1.43, 95% confidence interval=1.23-1.67) compared with those patients harboring the rs727088A allele. Moreover, functional relevance was further performed that individuals carrying the rs727088G allele were correlated with lower expression level of CD226 than individuals carrying the rs727088AA homozygous genotype. These findings indicated that functional polymorphism rs727088AG in CD226 might modify the susceptibility for the development of GC.

Background A number of case-control studies were conducted to investigate the association of SULT1A1 R213H polymorphisms with colorectal cancer (CRC) in humans. But the results were not always consistent. We performed a meta-analysis to examine the association between the SULT1A1 R213H polymorphism and CRC. Methods and Findings Data were collected from the following electronic databases: PubMed, Elsevier Science Direct, Excerpta Medica Database, and Chinese Biomedical Literature Database, with the last report up to September 2010. A total of 12 studies including 3,549 cases and 5,610 controls based on the search criteria were involved in this meta-analysis. Overall, no significant association of this polymorphism with CRC was found (H versus R: OR = 1.04, 95%CI = 0.94–1.16, P = 0.46; HR+HH versus RR: OR = 1.01, 95%CI = 0.92–1.11, P = 0.81; HH versus RR+HR: OR = 1.01, 95%CI = 0.74–1.38, P = 0.95; HH versus RR: OR = 1.00, 95%CI = 0.77–1.31, P = 0.98; HR versus RR: OR = 1.01, 95%CI = 0.92–1.11, P = 0.86). In subgroup analysis, we also did not find any significant association in Cauasians (H versus R: OR = 1.02, 95%CI = 0.92–1.15, P = 0.68; HR+HH versus RR: OR = 0.99, 95%CI = 0.91–1.09, P = 0.90; HH versus RR+HR: OR = 1.01, 95%CI = 0.73–1.39, P = 0.97; HH versus RR: OR = 0.99, 95%CI = 0.75–1.31, P = 0.94; HR versus RR: OR = 0.99, 95%CI = 0.90–1.09, P = 0.85). The results were not materially altered after the studies which did not fulfill Hardy-Weinberg equilibrium were excluded (H versus R: OR = 1.06, 95%CI = 0.95–1.19, P = 0.31; HR+HH versus RR: OR = 1.03, 95%CI = 0.93–1.13, P = 0.56; HH versus RR+HR: OR = 1.10, 95%CI = 0.78–1.56, P = 0.57; HH versus RR: OR = 1.09, 95%CI = 0.83–1.44, P = 0.53; HR versus RR: OR = 1.02, 95%CI = 0.92–1.13, P = 0.75). Conclusion This meta-analysis demonstrates that there is no association between the SULT1A1 R213H polymorphism and CRC.

Background and Objectives Tumor necrosis factor-α (TNF-α) plays a very important role in the development and progress of cancer. Some TNF-α polymorphisms have been confirmed to increase cancer risks; however, the association between TNF-α-238 polymorphism and cancers remains controversial and ambiguous. The aim of this study is to explore a more precise estimation of its relationship with cancer using meta-analysis. Methods Electronic searches of several databases were conducted for all publications on the association between this variant and cancer through March 2011. Odds ratios (OR) with 95% confidence intervals (95% CI) were used to access the strength of this association in the random-effect model. Results Thirty four studies with 34,679 cancer patients and 41,186 healthy controls were included. This meta-analysis showed no significant association between TNF-α-238 polymorphism and cancers (AA+GA vs GG: OR = 1.09, 95%CI = 0.88–1.34). In Caucasian and Asian subgroups, OR values (95% CI) were 1.14 (0.91–1.43) and 0.97 (0.58–1.61), respectively. In the subgroups of cancer type, no significant association was detected. The sensitivity analysis further strengthened the validity of these negative associations. No publication bias was observed in this study. Conclusions No significant association was found between the TNF-α-238 polymorphism and the risk for cancer.