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Abstract. Chemotherapy is one of the few effective choices for patients with advanced or recurrent gastric cancer (GC). However, the development of mutidrug resistance (MDR) to cancer chemotherapy is a major obstacle to the effective treatment of advanced GC. Additionally, the mechanism of MDR remains to be determined. In the present study, we tested IC 50 of cisplating (DDP), vincristine (VCR) and 5-fluorouracil (5-FU) in SGC7901, SGC7901/DDP and SGC7901/VCR gastric cancer cells using an MTT assay. The expression of let-7b and c-Myc in these cells was detected by qPCR and western blot analysis. The relationship between let-7b and c-Myc was explored using a luciferase reporter assay. Transfection of let-7b mimic or inhibitor was used to confirm the effect of let-7b on drug sensitivity in chemotherapy via the regulation of c-Myc expression. We found that the expression of let-7b was lower in chemotherapy-resistant SGC7901/DDP and SGC7901/VCR gastric cancer cells than that in chemotherapysensitive SGC7901 cells. By contrast, the expression of c-Myc was higher in SGC7901/DDP and SGC7901/VCR cells than that in SGC7901 cells. Furthermore, we confirmed that let-7b suppresses c-Myc gene expression at the mRNA and protein levels in a sequence-specific manner, while transfection of let-7b mimic increases drug sensitivity in chemotherapyresistant SGC7901/DDP and SGC7901/VCR cells by targeting downregulation of c-Myc. In SGC7901 drug-sensitive cells, however, the sensitivity of chemotherapy was significantly decreased following let-7b inhibitor transfection. The present study results demonstrated that let-7b increases drug sensitivity in chemotherapy-resistant SGC7901/DDP and SGC7901/VCR gastric cancer cells by targeting the downregulation of c-Myc and that, let-7b mimic reverses MDR by promoting cancer stem cell differentiation controlled by double-negative autoregulatory loops (Lin28/let-7 and Myc/let-7) and a double-positive autoregulatory loop (Lin28/Lin28B/Myc) existing in GC cells, which remains to be confirmed.

The relationship between egg consumption and breast cancer risk has been inconsistent, so it is necessary to conduct a meta-analysis to evaluate the relationship. PubMed, EMBASE and ISI Web of Knowledge were searched to find cohort studies or case control studies that evaluated the relationship between egg consumption and breast cancer risk. A comprehensive meta-analysis software was used to conduct the meta-analysis. 13 studies were included. The meta-analysis results showed that egg consumption was associated with increased breast cancer risk (RR 1.04, 95 % CI 1.01-1.08). Subgroup analyses showed egg consumption was also associated with increased breast cancer risk based on cohort studies (RR 1.04, 95 % CI 1.00-1.08), among European population (RR 1.05, 95 % CI 1.01-1.09), Asian population (RR 1.09, 95 % CI 1.00-1.18), postmenopausal population (RR 1.06, 95 % CI 1.02-1.10), and those who consumed ≥2, ≤5/week (RR 1.10, 95 % CI 1.02-1.17), but not in case-control studies (RR 1.06, 95 % CI 0.97-1.15), among American population (RR 1.04, 95 % CI 0.94-1.16), premenopausal population (RR 1.04, 95 % CI 0.98-1.11) and those who consumed ≥1, <2/week (RR 1.04, 95 % CI 0.97-1.11) or >5 eggs/week (RR 0.97, 95 % CI 0.88-1.06). Egg consumption was associated with increased breast cancer risk among the European, Asian and postmenopausal population and those who consumed ≥2, ≤5/week.

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