Alterations of Oral Microbiota in Chinese Patients With Esophageal Cancer.

Emerging evidence supports that oral microbiota are associated with health and diseases of the esophagus. How oral microbiota change in Chinese patients with esophageal cancer (EC) is unknown, neither is their biomarker role. For an objective to understand alterations of oral microbiota in Chinese EC patients, we conducted a case-control study including saliva samples from 39 EC patients and 51 healthy volunteers. 16S rDNA genes of V3-V4 variable regions were sequenced to identify taxon. Relationship between oral flora and disease was analyzed according to alpha diversity and beta diversity. Resultantly, the Shannon index (p = 0.2) and the Simpson diversity index (p = 0.071) were not significant between the two groups. Yet we still found several species different in abundance between the two groups. For the EC group, the most significantly increased taxa were Firmicutes, Negativicutes, Selenomonadales, Prevotellaceae, Prevotella, and Veillonellaceae, while the most significantly decreased taxa were Proteobacteria, Betaproteobacteria, Neisseriales, Neisseriaceae, and Neisseria. In conclusion, there are significant alterations in abundance of some oral microbiomes between the EC patients and the healthy controls in the studied Chinese participants, which may be meaningful for predicting the development of EC, and the potential roles of these species in EC development deserve further studies.

Patients With Reflux Esophagitis Possess a Possible Different Oral Microbiota Compared With Healthy Controls.

BACKGROUND AND AIM: Reflux Esophagitis (RE) is caused by a variety of factors including anatomical and functional alterations involved in the pathogenesis. Oral microbiota is influenced by many factors such as heredity, nutrition, environments and host conditions, but little is known about relationship between oral microbiota and RE. The aim of this study was to explore whether the oral microbiota is changed in patients with RE. METHODS: To clarify this correlation, fresh saliva samples from all subjects were collected and then oral microorganism diversity was analysed in 55 patients with RE and 51 controls via hypervariable tag sequencing and analyzing the V3-V4 region of the 16S rDNA gene. RESULTS: There was no difference found in oral microbial diversity between RE patients and healthy controls by Shannon diversity index (p=0.60) and Simpson diversity index (p= 0.38). The abundance of Proteobacteria was lower, but Bacteroidetes was higher in patients with RE at the phylum level. At the genus level the abundances of Prevotella, Veillonella, Megasphaera, Peptostreptococcus, Atopobium, Oribacterium, Eubacterium, and Lachnoanaerobaculum were increased, while Neisseria, Streptococcus, Rothia, Granulicatella, Gemella, Aggregatibacter, Treponema, Campylobacter, Filifactor, Corynebacterium, and Lactivibrio were decreased in RE patients than the controls. CONCLUSIONS: Our study suggested oral microbial dysbiosis in patients with RE, and identified bacterial species with potential biomarker significance. Further studies are required to understand role of oral microbial dysbiosis in the pathogenesis of RE.

Effects of hsa_circRBM23 on Hepatocellular Carcinoma Cell Viability and Migration as Produced by Regulating miR-138 Expression.

Primary hepatocellular carcinoma (HCC) is one of the most common malignant tumors. At present, the molecular mechanism of HCC remains unclear. A recent circular RNA (circRNA) profiling study showed that circRBM23 expression was upregulated in HCC tissues. Therefore, in this study, the impact of circRBM23 during the progression of HCC was evaluated. The expression levels of circRBM23 and miR-138 in HCC tissues and HCC cell lines were determined by RT-PCR and the results indicated that circRBM23 expression was increased in the HCC tissues and HCC cell lines, whereas miR-138 expression was decreased. An upregulation of circRBM23 expression in HCC cells was shown to increase cell viability, and also increased the ability of cells to migrate. Downregulation of circRBM23 was found to decrease cell viability, proliferation, and migration, and promote the expression of miR-138 and its related target genes, vimentin, and CCND3. Moreover, miR-138 was found to regulate HCC cell viability and migration, and the levels of vimentin and CCND3 protein expression were found to be inversely correlated with those of miR-138 expression. The downregulation of circRBM23 in HCC tissues can regulate the miR-138-mediated signal pathway by promoting miR-138 expression. The results in vivo demonstrated that circRBM23 is required for the tumorigenesis with downregulation of tumor suppressor miR-138. These data indicated that upregulated circRBM23 functioned as oncogene in HCC through regulating the tumor suppressor miR-138.