Search

Objective. In the research, the microbial changes in the tongue coating of patients with a damp phlegm pattern of gastric precancerous lesion (GPL) were investigated. Methods. This was a case-control study, in which 80 tongue coating samples were collected including 40 patients with a damp phlegm pattern of GPL, 20 patients with a nondamp phlegm pattern of GPL, and 20 healthy control people. The 16S rRNA microbiome technology was used to analyze the alterations of microorganisms in tongue coating of GPL patients with a damp phlegm pattern. Results. Microorganisms in the genus level were analyzed. Compared with the healthy control group, the relative abundance of 4 microorganisms (Solobacterium, Rothia, Oribacterium, and Alloprevotella) in the GPL group was significantly higher ( P < 0.05 ). The relative abundance of 10 microorganisms (Terrisporobacter, Solobacterium, Porphyromonas, Parvimonas, Lactobacillus, Johnsonella, Gemella, Fusibacter, Azoarcus, and Acidothermus) in the GPL damp phlegm pattern group was significantly lower than that in the GPL nondamp phlegm pattern group ( P < 0.05 ). In the comparison of phenotype “forms biofilms,” the relative abundance of microorganisms in the GPL group was significantly higher than that in the healthy control group ( P < 0.05 ). In the comparison of phenotype “contains mobile elements,” the relative abundance of microorganisms in the GPL damp phlegm pattern group was significantly lower than that in the GPL nondamp phlegm pattern group ( P < 0.05 ). In the comparison of microbial metabolic functions, the abundance ratio of “infectious diseases: bacterial” in the GPL group was significantly lower than that in the healthy control group ( P < 0.05 ). The abundance ratio of the “excretory system” and “folding, sorting, and degradation” in the GPL group was significantly higher than that in the healthy control group ( P < 0.05 ). Conclusions. Solobacterium may be a marker microorganism of the GPL damp phlegm pattern. The differential phenotype of microorganisms in tongue coating of the GPL damp tongue pattern is mainly reflected in “forms biofilms” and “contains mobile elements.”

BACKGROUND: Tongxie Yaofang is commonly used in the treatment of IBS-D. Many systematic reviews have confirmed its efficacy and safety, but the methodology and quality of evidence need to be further evaluated. METHODS: The databases of Chinese National Knowledge Infrastructure (CNKI), Chinese Biomedical Literature (CBM), Wanfang, VIP, Web of Science (SCI), PubMed, Cochrane Library, and Embase were searched to gather systematic evaluations of TXYF in treating IBS-D. The search time was from inception to January 2021. The search was performed independently by 2 researchers who screened the literature and extracted data. Methodological quality of the studies included in the systematic evaluation was evaluated by the A MeaSurement Tool to Assess systematic Reviews-2 (AMSTAR-2) scale. The Grading of Recommendations, Assessment, Development and Evaluations (GRADE) system was used to categorize the evidence quality of outcome indicators, and the curative effect evaluation was summarized. RESLUTS: A total of 10 systematic evaluations were included, and the results of AMSTAR-2 evaluation showed that 6 reports were relatively complete, 4 reports were poor, and the overall quality was not high. DISCUSSION: It was revealed that TXYF can improve the total clinical effective rate and symptoms of patients with IBS-D, but the GRADE evaluation results showed that the quality of evidence was low to extremely low. It is suggested that further high-quality clinical research should be conducted to provide more reliable evidence-based medical evidence for the application of TXYF in the treatment of irritable bowel syndrome.

YAP1 is a core protein of the Hippo signaling pathway and is associated with malignancy and immunosuppression. In the present study, we discovered a novel lncRNA, RP11-323N12.5, with tumor promotion and immunosuppression activities through enhancing transcription of YAP1. RP11-323N12.5 was identified using GEPIA. Its expression levels and their relationship with clinical features were investigated using clinical samples. The regulation of YAP1 transcription by RP11-323N12.5 was investigated in both GC and T cells, the tumor and immunosuppression promotion roles of RP11-323N12.5 were explored in vitro and in vivo. RP11-323N12.5 was the most up-regulated lncRNA in human GC, based on data from the TCGA database. Its transcription was significantly positively correlated with YAP1 transcription, YAP1 downstream gene expression which contribute to tumor growth and immunosuppression. RP11-323N12.5 promoted YAP1 transcription by binding to c-MYC in the YAP1 promoter region. Meanwhile, transcription of RP11-323N12.5 was also regulated by YAP1/TAZ/TEADs activation in GC cells. RP11-323N12.5 had tumor- and immnosuppression-promoting effects by enhancing YAP1 downstream genes in GC cells. Excessive RP11-323N12.5 was also observed in tumor-infiltrating leukocytes (TILs), which may be exosome-derived and also be related to enhanced Treg differentiation as a result YAP1 up-regulation. Moreover, RP11-323N12.5 promoted tumor growth and immunosuppression via YAP1 up-regulation in vivo. RP11-323N12.5 was the most up-regulated lncRNA in human GC and it promoted YAP1 transcription by binding to c-MYC within the YAP1 promoter in both GC and T cells. RP11-323N12.5 is an ideal therapeutic target in human GC due to its tumor-promoting and immunosuppression characteristics.

Background/aims ErbB3 is an oncogene which has proliferation and metastasis promotion effects by several signaling pathways. However, the individual expression difference regulated by miRNA was almost still unknown. We focused on the miRNAs associated SNPs in the 3′-UTR of ErbB3 to investigate the further relationship of the SNPs with miRNAs among Chinese gastric cancer (GC) patients. Methods We performed case–control study including 851 GC patients and 799 cancer-free controls. Genotyping, real-time PCR assay, cell transfection, the dual luciferase reporter assay, western-blot, cell proliferation and trans-well based cell invasion assay were used to investigate the effects of the SNP on ErbB3 expression. Moreover, a 5-years-overall survival and relapse free survival were investigated between different genotypes. Results We found that patients suffering from Helicobacter pylori (Hp.) infection indicated to be the susceptible population by comparing with controls. Besides, SNP rs3202538 (G/T) in ErbB3 3′-UTR was involved in the occurrence of GC by acting as tumor risk factors. SNP rs3202538 (G/T) could be regulated by both miR-204 and miR-211 which caused an upregulation of ErbB3 in patients. Furthermore, the carriers of T genotype was related to the significantly high expression of ErbB3, and to big tumor size, poor differentiation as well as the high probability of metastasis. Both miR-211 and miR-204 can significantly decrease cell proliferation, metastasis as well as downstream AKT activation through G but not T allele of ErbB3 3′UTR. Moreover, the SNP of G/T was associated with shorter survival of post-surgery GC patients with 5 years of follow up study. Conclusion In conclusion, our findings have shown that the SNP rs3202538 (G/T) in ErbB3 3′-UTR acted as promotion factors in the GC development through disrupting the regulatory role of miR-204 and miR-211 in ErbB3 expression. Electronic supplementary material The online version of this article (doi:10.1186/s12935-017-0449-z) contains supplementary material, which is available to authorized users.

Background Recently the roles of circRNAs were extensively studied within human malignancies. Now we explored a potential regulatory axis consisted of circ-STAT3.46-miR-139-5p-IGF1R in human colon cancer. Methods The expression of circ-STAT3.46-miR-139-5p-IGF1R were determined by using real-time PCR in human colon cancer (n=56) and adjacent normal tissues. The relationship between clinical characters and tissue or serum exosome circ-STAT3.46 were studied. The detailed regulation within circ-STAT3.46-miR-139-5p-IGF1R was verified by in vitro studies. Results Aberrant expression of circ-STAT3.46, miR-139-5p, and IGF1R were spotted between colon cancer tissues and control. A significantly negative correlation between circ-STAT3.46 and miR-139-5p were verified within human colon cancer tissues. Expression of circ-STAT3.46 in colon cancer tissue and serum exosome were associated with TMN stage and bad prognosis of post-surgery colon cancer patients. IGF1R was positively correlated to circ-STAT3.46 in human colon cancer tissues. Moreover, the transcription of circ-STAT3.46 was regulated by IGF1/IGF1R/STAT3 signaling. Overexpression of circ-STAT3.46 can decrease miR-139-5p in colon cancer cells, meanwhile, increased miR-139-5p were found in circ-STAT3.46 knockdown cells. RNA pull-down assay revealed that circ-STAT3.46 could sponge miR-139-5p, and luciferase reporter assay indicated that miR-139-5p could further downregulate IGF1R transcription by binding to its 3'UTR in human colon cancer cells. Conclusions circ-STAT3.46 was regulated by IGF/IGF1R/STAT3 activation, and overexpression of circ-STAT3.46 can up-regulate IGF1R by sponging of miR-139-5p within human colon cancer.