Edited by Varda Rotter Keywords:Cancer associated fibroblasts microRNA Protein tyrosine phosphatase and tensin homologue Gastric cancer a b s t r a c t It is well established that the interaction between cancer cells and microenvironment has a critical role in tumor development, but the roles of miRNAs in this interaction are rarely known. Here, we have shown that miR-106b is up-regulated in cancer associated fibroblasts compared with normal fibroblasts established from patients with gastric cancer, the expression level of miR-106b is associated with poor prognosis of patients, and CAFs with down-regulated miR-106b could significantly inhibit gastric cancer cell migration and invasion by targeting PTEN. Taken together, these data suggest that miR-106b might be a novel candidate target for the treatment of gastric cancer.

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BackgroundThe aim of this study was to investigate the differences and influencing factors for postsurgical gastroparesis syndrome incidence after laparoscopic and open radical gastrectomy.MethodsClinical data were collected for 563 patients who underwent open radical gastrectomy for gastric cancer and 72 cases receiving laparoscopic radical gastrectomy. We retrospectively analyzed the incidence of postsurgical gastroparesis syndrome, clinical features, course of disease, and risk factors of these two groups.ResultsThere was no statistical difference for the incident rate of postsurgical gastroparesis syndrome between laparoscopic and open radical gastrectomy (6.9% vs. 3.7%, P > 0.05). Preoperative outflow tract obstruction and Billroth II anastomosis were the two risk factors for postsurgical gastroparesis syndrome in the open radical gastrectomy group and the laparoscopic surgery for gastric cancer group. The same results were obtained from logistic regression statistical analysis. Age greater than 70 years was also one of the risk factors for postsurgical gastroparesis syndrome in the open radical gastrectomy group (P < 0.05).ConclusionsLaparoscopic radical gastrectomy for gastric cancer does not increase the incident rate of postsurgical gastroparesis syndrome.

Mounting evidence indicates that alterations in the intestinal microbiota may be associated with neurological disorders such as multiple sclerosis (MS). MS is a putative autoimmune disease of the central nervous system. However, it has not been determined whether the intestinal microbiota and host immune status are altered in Chinese patients with stable MS. In our study, 22 Chinese patients with stable MS and 33 healthy controls were enrolled for fecal microbiota analysis and host immunity evaluation. The microbial diversity and composition, bacterial co-occurrence correlations, predictive functional profiles, and microbiota-cytokine correlations between the two groups were compared. We observed that while the overall structure of the fecal microbiota did not change significantly, the abundances of several key functional bacteria, primarily Faecalibacterium, decreased remarkably. Faecalibacterium and Granulicatella could be used to distinguish between patients with MS and healthy controls with an area under the curve of 0.832. PiCRUSt analysis revealed that genes associated with fructose, mannose, and fatty acid metabolism were significantly enriched in the MS microbiota. In addition, we also observed that the levels of several pro- and anti-inflammatory cytokines and chemokines, such as IL-1ra, IL-8, IL-17, and TNF-α changed observably, and the abundances of key functional bacteria like butyrate producers correlated with the changes in the cytokine levels. Our present study indicated that altered composition of the fecal microbiota might play vital roles in the etiopathogenesis of MS by regulating host immunity, which suggests that microbiota-targeting patient-tailored early intervention techniques might serve as novel therapeutic approaches for MS.

Background/Aims: Long noncoding RNAs (lncRNAs) constitute a large proportion of noncoding transcripts that have recently emerged as a new class of important regulators in cancers. LncRNA BCYRN1, also known as BC200, has a potential function in tumorigenesis. However, the clinical significance of BCYRN1 and its effect on colorectal cancer (CRC) progression remains unclear. Methods: Quantitative reverse transcriptase PCR (qRT-PCR) was performed to investigate the expression of BCYRN1 in CRC tissues and cell lines. The biological function of BCYRN1 was also investigated through knockdown and overexpression of BCYRN1 in vitro. Microarray bioinformatics analysis was performed to analyze the putative targets of BCYRN1. Results: The results showed that BCYRN1 expression was significantly upregulated in 96 CRC tumor tissues compared with para-carcinoma control tissues. Additionally, BCYRN1 overexpression was associated with larger tumor size and advanced pathological stages in CRC patients. In vitro BCYRN1 knockdown significantly inhibited the proliferation and apoptosis of CRC cells. Furthermore, NPR3 was identified to be a target of BCYRN1 and was downregulated by BCYRN1 knockdown. Conclusion: Together, we provide the first evidence that BCYRN1 plays an oncogenic role in CRC cells. BCYRN1 may be a promising prognostic biomarker and a potential therapeutic target for CRC.

Long noncoding RNAs (lncRNAs) have emerged as regulators in a variety of biological processes, including carcinogenesis in human cancer. UCA1 has been reported to be upregulated in gastric cancer (GC); however, the underlying functional roles of UCA1 in GC have not been established. In the current study, we showed that UCA1 is significantly higher in GC tissues and cells compared with adjacent normal tissues and a gastric epithelium cell line, respectively. Higher UCA1 expression was associated with lymph node metastasis, TNM stage, and poor overall survival (OS) in GC patients. In vitro functional studies confirmed that UCA1 promotes cell proliferation, colony formation ability, and cell invasion in GC cells. We demonstrated that knockdown of UCA1 inhibits tumor growth in vivo. The double luciferase reporter, RNA‐binding protein immunoprecipitation assay, and RNA pull down assay demonstrated that miR‐590‐3p serves as a target for UCA1. UCA1 promoted cell proliferation and invasion by negatively regulating miR‐590‐3p expression. Moreover, we demonstrated that CREB1 is a downstream target of miR‐590‐3p and UCA1 activates CREB1 expression by sponging to miR‐590‐3p. Thus, these results showed that UCA1 functions as an oncogene in GC and may be a target for treatment of GC.

Introduction Obesity has an unclear pathogenesis. MicroRNAs (miRNAs) may function as biologically active molecules for obesity through regulating adipocyte differentiation. This study aimed to identify how miR-129-5p (a specific miRNA) regulates adipogenesis in vitro and explore its possible role in the pathogenesis of obesity in humans. Materials and Methods The miR-129-5p expression was detected in obese mouse models. The effect of miR-129-5p on adipocyte differentiation was observed, and the adipose markers were analyzed. Bioinformatics and dual-luciferase reporter assay were applied to predict and confirm the target genes of miR-129-5p. The human serum samples were detected and analyzed. Results miR-129-5p is highly expressed in adipose tissues of db/db mice. Gain- and loss-of-function studies show that miR-129-5p could significantly inhibit adipocyte differentiation and white adipocyte browning in vitro and decreases the level of specific markers, such as FABP4, UCP1, and PPARγ, in mature white and brown adipocytes. miR-129-5p directly targets ATG7 which is predicted with bioinformatics and confirmed by dual-luciferase reporter assay. Serum miR-129-5p level was evidently elevated in patients with simple obesity (p < 0.01) and correlates with obesity indices, including BMI (r = 0.407, p < 0.029) and fat percentage (r = 0.394, p < 0.038). Conclusion miR-129-5p might target on the ATG7-related autophagy signaling network that regulates white and brown adipogenesis. Importantly, the aforementioned results suggest serum miR-129-5p might be a potential biomarker and therapeutic target for obesity.

Increased VFA independently predicts surgical complications in patients after gastrectomy. However, VFA is not a prognostic biomarker of OS or DFS in patients with gastric cancer.