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Background Gastric cancer is the second most common cause of death from cancer worldwide. Epidemiologic studies have examined the possible association between tomato products consumption and gastric cancer, but the relationship between tomato products and the risk of gastric cancer is controversial. We performed a meta-analysis of cohort and case–control studies to analyze this association. Methods We systematically searched MEDLINE and EMBASE and contacted authors to identify potential studies published from January 1966 to June 2012. We pooled the relative risks from individual studies using a random-effects model and performed heterogeneity and publication bias analyses. Results Twenty-one studies were eligible for our inclusion criteria, in a pooled analysis of all studies, consumption of large amounts of tomato products (in a comparison of the highest and lowest consumption groups) reduced the risk for gastric cancer (odds ratio, 0.73; 95% confidence interval, 0.60–0.90). The pooled OR of lycopene consumption and serum lycopene was 0.88 (95% CI = 0.67–1.16) and 0.79 (95% CI = 0.59–1.07), respectively. Conclusions Consumption of large amounts of tomato products is associated with a reduced risk of gastric cancer. However, because of potential confounding factors and exposure misclassification, further studies are required to establish these findings.

AIM: To investigate the effects of proliferation and apoptosis induced by cyclooxygenase-2 (COX-2) inhibitor celecoxib in combination with cisplatin. METHODS: The human pancreatic cancer cell line BxPC-3 cells were treated with COX-2 inhibitors celecoxib and cisplatin. The cell relative viability was examined using 3 (4, 5-dimethylethiazoly 1-2-) 2, 5-diphonyl tetrazolium bromide (MTT) assays. the expression of COX-2 mRNA was detected by RT-PCR, flow cytometry and Hoechst-33258 were used to demonstrate apoptotic changes in celecoxib and cisplatin treated cells. RESULTS: After treatment of BxPC-3 cells with celecoxib, as measured by MTT, cell viability was inhibited in a dosedependent and time-dependent manner with an IC50 of 100 nM at the time of 24h. The expression of COX-2 mRNA could be significantly decreased by celecoxib. Furthermore, we demonstrated that the combination of celecoxib with cisplatin inhibited cell growth and induced cell apoptosis to a greater degree than either compound alone. The apoptotic morphologies were demonstrated by Hoechst-33 258. CONCLUSION: Combination of celecoxib with cisplatin inhibits cell proliferation and induces cell apoptosis, and the potent effectiveness of celecoxib in combination with gemcitabine may hold a promise in the clinical treatment of pancreatic cancer. Liu JW, Li KZ, Dou KF, Song ZS, Su MQ, Yu WB. Effects of COX-2 inhibitor with cisplatin on proliferation and apoptosis of pancreatic cancer cells. Shijie Huaren Xiaohua Zazhi 2004;12(5):1139-1143

Background MicroRNAs are a class of small non-coding RNAs that play an important role in various human tumor initiation and progression by regulating gene expression negatively. The aim of this study was to investigate the effect of miR-214 on cell proliferation, migration and invasion, as well as the functional connection between miR-214 and PTEN in gastric cancer. Methods miR-214 and PTEN expression was determined in gastric cancer and matched normal tissues, and human gastric cancer cell lines by quantitative real-time PCR. The roles of miR-214 in cell proliferation, migration and invasion were analyzed with anti-miR-214 transfected cells. In addition, the regulation of PTEN by miR-214 was evaluated by Western blotting and luciferase reporter assays. Results miR-214 was noted to be highly overexpressed in gastric cancer tissues and cell lines using qRT-PCR. The expression level of miR-214 is significantly associated with clinical progression and poor prognosis according to the analysis of the clinicopathologic data. We also found that the miR-214 levels are inversely correlated with PTEN in tumor tissues. And PTEN expression level is also associated with metastasis and invasion of gastric cancer. In addition, knockdown of miR-214 could significantly inhibit proliferation, migration and invasion of gastric cancer cells. Moreover, we demonstrate that PTEN is regulated negatively by miR-214 through a miR-214 binding site within the 3’-UTR of PTEN at the posttranscriptional level in gastric cancer cells. Conclusions These findings indicated that miR-214 regulated the proliferation, migration and invasion by targeting PTEN post-transcriptionally in gastric cancer. It may be a novel potential therapeutic agent for gastric cancer.