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Sarcomas are a broad family of cancers that arise from cells of mesenchymal origin in virtually every tissue of the body. Some transcription factors (TFs) have been reported to be involved in the pathogenesis and metastasis of sarcomas. The expression of certain long noncoding RNAs (lncRNAs) has been correlated with the degree of cancer prognosis. There is an urgent need to effectively integrate TFs and lncRNA/microRNA/mRNA regulatory axis and further identify more key regulators that play crucial roles in sarcomas. We performed a network-based computational analysis to investigate the lncRNA-TF cross talks via integrating lncRNA-TF ceRNA interactions and TF-TF protein-protein interactions. Multiple topology analyses were performed to the sarcomas-related global lncRNA-TF network. Several lncRNAs or TFs with central topology structures were identified as key regulators and used to locate a hub-associated lncRNA-TF subnetwork. Three functional modules were identified from the sarcomas-related global lncRNA-TF network, which have shown significant pathway enrichment and prognosis capability. The lncRNAs and TFs of these modules were shown to participate in sarcoma-related biological phenomena through involving in mitogen-activated protein kinases (MAPK), Jak-STAT, and transforming growth factor (TGF-beta) signaling pathways. More importantly, a subset of core lncRNA-TF cross talks that might form positive feedback loops to control biological processes of sarcomas was identified. These core lncRNA-TF positive feedback loops showed more TF binding affinity than other lncRNAs. All the results can help us uncover the molecular mechanism of sarcomas and provide a novel way for diagnosis biomarker and therapeutic target identification.

This study aimed to explore the role of obestatin R gene-related protein (OB-RGRP) in autocrine signal transduction of adipocytes. Primary rat adipocytes were isolated and verified by microscopic observation and oil red O staining. OB-RGRP expression vector and OB-RGRP siRNA (si-OB-RGRP) were constructed and transfected into adipocytes. Adipocytes were then divided into five groups: (1) Control; (2) Vector (empty expression vector); (3) OB-RGRP (OB-RGRP expression vector); (4) si-OB-RGRP NC (si-OB-RGRP negative control); (5) si-OB-RGRP. mRNA and protein levels of OB-RGRP, JAK2, phosphorylated JAK2 (p-JAK2), STAT3 and phosphorylated STAT3 (p-STAT3) were examined using RT-PCR and western blot, respectively. Results showed that mRNA and protein levels of OB-RGRP in the Vector and si-OB-RGRP NC groups were similar to those in the Control group. Their levels in the si-OB-RGRP and OB-RGRP groups were significantly down-regulated and up-regulated (

Objective This study investigated the effects of leptin on intestinal flora and inflammation in mice with high-fat diet (HFD)-induced obesity. Methods Mice were fed an HFD for 8 weeks; some were concurrently administered oral leptin for 4 weeks. Pathological changes in adipose tissue were detected using hematoxylin–eosin staining; endotoxin content in adipose tissue was measured by enzyme-linked immunosorbent assay. Intestinal flora were characterized by 16S bacterial rDNA sequencing. Levels of Toll-like receptor 4 (TLR4), nuclear factor-κB inhibitor α (IκB-α), and phosphorylated c-Jun N-terminal kinase (p-JNK) were detected by western blotting. Results Mice in the HFD group exhibited weight gain, elevated endotoxin content, and adipocyte hypertrophy, compared with the non-obese control group. Moreover, abundance of bacteria in the Bacteroides genus and community diversity were both reduced in the HFD group; reductions also were observed at corresponding phylum, class, and order levels. Levels of TLR4, IκB-α, and p-JNK were also elevated in the HFD group. Compared with the model group, leptin administration reduced the weight gain and endotoxin content, while increasing Bacteroides abundance and community diversity; it also reduced the levels of TLR4, IκB-α, and p-JNK. Conclusion Leptin administration improved intestinal flora dysfunction and inflammation in mice with HFD-induced obesity.

Jun Rong,1,* Qian Wang,2,* Yanzhou Zhang,1 Daolong Zhu,1 Handong Sun,2 Weiwei Tang,3 Rongping Wang,1 Weihong Shi,3 Xiu-feng Cao1,2 1Department of Thoracic surgery, Taikang Xianlin Drum Tower Hospital, School of Medicine, Nanjing University, 2Department of Oncology Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, China; 3Department of Clinical Medicine, Jiangsu Vocational College of Medicine, Yancheng, China *These authors contributed equally to this work Background: Circular RNAs (circRNAs) are a class of noncoding RNAs with closed loop structures. There has been growing evidence showing that circRNAs are involved in the pathogenesis of human diseases including various carcinomas. Our study is aimed to investigate the association between a new circRNA named circ-DLG1 (hsa_circ_0007203) and esophageal squamous cell carcinoma (ESCC) carcinogenesis. Methods: The circ-DLG1 expression levels were detected by real-time quantitative reverse transcription-polymerase chain reaction in cells, tissues, and plasmas. The correlation between circ-DLG1 expression and clinicopathologic features was then analyzed. The effect of circ-DLG1 expression on cell proliferation was evaluated in vitro by CCK8 assay and clone formation experiment. Finally, a network of circ-DLG1 with its targeted miRNA interactions and corresponding mRNAs was constructed. Results: circ-DLG1was found to be significantly upregulated in ESCC cells, tissues, and plasmas compared to normal cases. Furthermore, in vitro assays, TE10 and KYSE180, of the ESCC cell lines demonstrated that knockdown of circ-DLG1 reduced cell proliferation significantly. Prediction and annotation revealed that circ-DLG1 was able to sponge to 20 miRNAs and 60 corresponding target mRNAs. Conclusion: Our study indicated that upregulation of circ-DLG1 promoted esophageal cell proliferation ability and might serve as a novel biomarker for ESCC. Keywords: ESCC, spong, upregulation, biomarker, miRNAErratumfor this paper has been published&nbsp

Rationale: A 27-year-old woman with a history of systemic lupus erythaematosus (SLE) developed hemophagocytic syndrome (HPS) secondary due to an unrecognized infection that led to severe SLE with a prolonged recovery. Patient concerns: The patient showed a high spiking fever and myalgia. Laboratory data revealed pancytopenia and immunological abnormalities. Pulse methylprednisone plus intravenous immunoglobulin (IVIG) failed to improve the clinical symptoms and laboratory data. Diagnoses: As activated macrophages with hemophagocytosis were confirmed in bone marrow histology, the patient was diagnosed as having reactive HPS. Interventions and outcomes: Her reactive HPS was successfully treated with intravenous antibiotics and was followed by oral prednisolone and hydroxychloroquine maintenance therapy. Lessons: In severe SLE, patients with persistent high fever, cytopenia, and elevated levels of serum ferritin and liver enzymes should be strongly suspected of reactive HPS, and aggressive examination, such as bone marrow biopsy, needs to be considered for early diagnosis and proper treatment.

Dysregulation of cyclin A1 (CCNA1) is implicated in the carcinogenesis, progression and metastasis of many types of solid tumours. In the present study, an mRNA single-channel expression profile chip experiment revealed that the CCNA1 mRNA levels in oesophageal squamous cell carcinoma (ESCC) were increased >10-fold compared with those in the adjacent non-cancer tissues. Reverse transcription-quantitative polymerase chain reaction and immunohistochemistry analyses were performed to additionally investigate the role of CCNA1 in the development and progression of ESCC in patients treated by radical resection of the oesophagus. The association between CCNA1 mRNA expression and the clinicopathological parameters of patients with ESCC was statistically analysed. The results indicated that upregulation of CCNA1 occurred in ~70% of patients with ESCC, and increased CCNA1 mRNA expression was significantly associated with advanced clinical stage, lymph node metastasis, invasiveness and poor clinical outcome, including disease-free survival and overall survival rates. Taken together, the data suggested that CCNA1 had an important function in ESCC development and progression, and may serve as a prognostic biomarker and therapeutic target in ESCC.

Objective We explored the association between single nucleotide polymorphisms (SNPs) rs207454 and rs494852 located in xanthine dehydrogenase (XDH) and gastric cancer (GC) survival. Methods A total of 940 patients with gastric cancer were enrolled and genotyped using TaqMan allelic discrimination method. The Kaplan–Meier test and log-rank examine were used to assess the effect of genetic variation. Results Patients carrying rs207454 CC genotype had a longer survival time than those with the AA genotype (P = 0.042). The similar association was detected in the recessive model (P = 0.017). We conducted expression quantitative trait loci (eQTL) analysis and found that gastric cancer patients carrying rs207454 CC genotype had significant lower XDH levels than those with AA/AC genotype, suggesting that rs207454 polymorphism effected the expression of XDH. Additionally, the Kaplan-Meier curves showed that gastric cancer patients with high expression of XDH had remarkably poor survival outcome than those with low expression (hazard ratio [HR] = 1.53, 95% confidence interval [CI] = 1.29–1.82). Conclusions Genetic variants in XDH were associated with the survival of gastric cancer and may act as prognostic markers for individual suffered from gastric cancer.

The aim of this study was to determine whether in vitro fertilization (IVF) outcomes are associated with inherited thrombophilias.Several databases including PubMed, Embase, and Cochrane Library were retrieved up to 12 January 2016. The quality of the included studies was assessed by two authors. The associations of the following mutations in inherited thrombophilias and IVF outcomes were explored: factor V Leiden (FVL), prothrombin gene G20210A mutation (PGM), 5,10-methylentetrahydrofolate reductase (MTHFR) C677T, MTHFR (A1298C) and activated protein C resistance (APCR). The main outcome measures included CPR and implantation rate (IR). The relative risk (RR) and its 95 % confidence interval (CI) were calculated for effect index. Heterogeneity test was evaluated by Chi-square based on Q statistic and I (2) statistics.A total of seven articles published between 2007 and 2015 with the ages of subjects between 30.9 and 36.2 were included. For subgroups analysis of CPR or IR, there were no significant differences in MTHFR (C377T), MTHFR (A1298C), FVL, PGM, and FVL/PGM mutation were found between the mutation group and control group (P 0. 05).IVF outcomes are not associated with FVL, PGM, MTHFR (C677T), MTHFR (A1298C), and APCR mutation in inherited thrombophilias.

Background In the past decades, a good deal of studies has provided the possibility of the circulating microRNAs (miRNAs) as noninvasive biomarkers for cancer diagnosis. The aim of our study was to detect the levels of circulating miRNAs in tissues and plasmas of gastric cancer (GC) patients and evaluate their diagnostic value. Methods Tissue samples were collected from 85 GC patients. Plasma samples were collected from 285 GC patients and 285 matched controls. Differentially expressed miRNAs were filtered with by Agilent Human miRNA Microarray and TaqMan low density array (TLDA) with pooled samples, followed by the quantitative reverse transcription polymerase chain reaction (qRT-PCR) validation. Receiver operating characteristic (ROC) curves were structured to evaluate the diagnostic accuracy of the miRNAs. The plasma level of miR-26a in GC patients of different clinical stages was compared. Results Four miRNAs (miR-26a, miR-142-3p, miR-148a, and miR-195) revealed coincidentally decreased levels in tissue and plasma of the GC patients compared with controls, and ROC curves were constructed to demonstrate that miR-26a had a highest area under the ROC curve (AUC) of 0.882. Furthermore, miR-26a was stably detected in the plasma of GC patients with different clinical characteristics. Conclusion Plasma miR-26a may provide a novel and stable marker of gastric cancer.