There is an increasing movement against use of antibiotic growth promoters in animal feed. Prebiotic supplementation is a potential alternative to enhance the host's natural defense through modulation of gut microbiota. In the present study, the effect of mannan oligosaccharide (MOS) and virginiamycin (VIRG) on cecal microbial ecology and intestinal morphology of broiler chickens raised under suboptimal conditions was evaluated. MOS and VIRG induced different bacterial community structures, as revealed by denaturing gradient gel electrophoresis of 16S rDNA. The antibiotic treatment reduced cecal microbial diversity while the community equitability increased. A higher bacterial diversity was observed in the cecum of MOS-supplemented birds. Quantitative polymerase chain reaction results indicated that MOS changed the cecal microbiota in favor of the Firmicutes population but not the Bacteroidetes population. No difference was observed in total bacterial counts among treatments. MOS promoted the growth of Lactobacillus spp. and Bifidobacterium spp. in the cecum and increased villus height and goblet cell numbers in the ileum and jejunum. These results provide a deeper insight into the microbial ecological changes after supplementation of MOS prebiotic in poultry diets.

Human immediate early response 2 (IER2) has been reported to function as a potential transcriptional factor or transcriptional co‑activator and seems to play a pivotal role in tumor cell motility and metastasis, however, its role and underlying mechanisms in hepatocellular carcinoma (HCC) remain unknown. Herein, we demonstrated that overexpression of IER2 in HCC cells increased cell adhesion to fibronectin, migration and invasion, whereas knockdown of IER2 displayed the opposite effects. In agreement with this phenotype, IER2 expression was positively correlated with the metastatic potential and integrin β1 (ITGB1) expression in HCC cell lines. Moreover, we demonstrated a critical role for IER2 in regulation of HCC cell‑extracellular matrix (ECM) adhesion and motility by the transcriptionally promoted ITGB1. Furthermore, we showed that ITGB1‑focal adhesion kinase (FAK)‑Src‑paxillin signal pathway activated by IER2 may contribute to the HCC cell‑ECM adhesion and motility. These results demonstrated that IER2 promoted HCC cell adhesion and motility probably by directly increasing ITGB1 expression and subsequently activating the ITGB1‑FAK‑Src‑paxillin signal pathway.

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The recurrence and metastasis of hepatocellular carcinoma (HCC) are a major concern in current research. Epithelial-mesenchymal transition (EMT) is the leading cause underlying the high mobility and invasiveness of tumor cells. Myricetin is a natural flavonol with various pharmacological activities. The effects of myricetin on the migration and invasion of HCC MHCC97H cells were evaluated in the present study. Wound healing, Transwell migration and invasion assays were used to examine cell migration and invasion. Western blot analysis and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) were used to examine the expression of epithelial (E)-cadherin, neural (N)-cadherin and vimentin. The present study aimed to investigate the effects of myricetin on the migration and invasion of HCC MHCC97H cells. It was indicated that myricetin decreased the viability of MHCC97H cells in a concentration and time-dependent manner, and inhibited MHCC97H cells migration and invasion. As the concentration of myricetin increased, filopodia and lamellipodia in cells weakened and cells were arranged more closely. RT-qPCR and western blotting revealed that myricetin upregulated E-cadherin expression and downregulated N-cadherin. Collectively, the results of the present study demonstrate that myricetin may inhibit the migration and invasion of HCC MHCC97H cells by inhibiting the EMT process.