Increasing evidence has indicated that long non-coding RNAs (lncRNAs) serve an essential role in carcinogenesis and cancer development. It has been reported that lncRNA nicotinamide nucleotide transhydrogenase antisense RNA 1 (NNT-AS1) serves a crucial role in several types of cancer. However, the clinical significance of circulating NNT-AS1 expression in colorectal cancer (CRC) remains to be elucidated. The current study aimed to investigate the potential role of NNT-AS1 and the clinical significance of its serum expression levels in patients with CRC. The expression of NNT-AS1 was measured in 40 pairs of tumor and adjacent normal tissues from patients with CRC via reverse transcription-quantitative PCR. The serum expression levels of NNT-AS1 were assayed in an independent cohort of healthy controls and patients with CRC. The levels of NNT-AS1 were also compared between paired preoperative and postoperative serum samples. In addition, the presence of exosomal NNT-AS1 in serum was explored. Furthermore, the biological roles of NNT-AS1 were investigated in CRC cells in vitro. The expression of NNT-AS1 was significantly upregulated in tumor tissues compared with adjacent normal tissues (P<0.05). A higher level of NNT-AS1 was associated with an advanced CRC stage. The serum levels of NNT-AS1 were significantly upregulated in patients with CRC compared with healthy subjects (P<0.05). Furthermore, the NNT-AS1 levels were significantly decreased in postoperative samples compared with preoperative samples (P<0.01). In addition, it was also identified that NNT-AS1 was upregulated in CRC exosomes (P<0.01), whereas no significant difference was observed in NNT-AS1 levels between serum and exosomes. Silencing of NNT-AS1 inhibited the proliferation, migration and invasion of CRC cells. It was also identified that NNT-AS1 exerted its effects via regulation of the microRNA-496/Ras-related protein Rap-2c axis. The present study demonstrated that circulating NNT-AS1, which may be protected by exosomes, could be a novel potential biomarker and therapeutic target in CRC.

Fibronectin type III domain-containing protein 1 (FNDC1) is a protein that contains a major component of the structural domain of fibronectin. Although many studies have indicated that FNDC1 serves vital roles in the development of various diseases, the role of FNDC1 in the progression of breast cancer (BC) remains elusive. The aim of the present study was to investigate the biological functions of FNDC1 in BC cells and the associated mechanisms. The expression levels of FNDC1 in BC tissues and normal breast tissues were analyzed using The Cancer Genome Atlas database (TCGA). Kaplan-Meier curves were mined from TCGA to examine the clinical prognostic significance of FNDC1 mRNA in patients with BC. The expression of FNDC1 was knocked down by transfection with shRNA in BC cells. Cell viability, colony formation ability, migration and invasion were assayed following the silencing of FNDC1 in BC cells. The expression of proteins was measured using a western blotting assay. The bioinformatic data indicated that the FNDC1 mRNA expression levels were significantly upregulated in BC tissues compared with normal breast tissues, and the high mRNA expression levels of FNDC1 were associated with a lower overall survival in patients with BC. The downregulation of FNDC1 inhibited the proliferation, colony formation, migration and invasion of BC cells. Investigation of the mechanisms revealed that the silencing of FNDC1 decreased the protein expression levels of MMPs and epithelial-to-mesenchymal markers. Furthermore, the silencing of FNDC1 led to the inactivation of the PI3K/Akt signaling pathway. FNDC1 was highly upregulated and acted as an oncogene in BC. Therefore, targeting FNDC1 may be a potential strategy for the treatment of BC.

Background: Nonalcoholic steatohepatitis (NASH) is a common liver injury which will develop into advanced fibrosis and cirrhosis. This study was designed to identify the different serum metabolites of NASH hamsters and predict the diagnosis biomarkers for NASH. background: Nonalcoholic steatohepatitis (NASH) is the second leading cause of liver transplantation for hepatocellular carcinoma. In this study, metabonomics was used to identify the serum differential metabolites to study the relationship between metabolites and pathogenesis of NASH. Material and methods: Golden hamsters were randomly divided into a control group that received a normal diet and a NASH group that received a high-fat diet (HFD). After 12 weeks of feeding, the body and liver weight of the hamsters were monitored. Serum biochemical parameters and liver histopathological changes were analyzed. Moreover, an untargeted metabolomics analysis based on a GC-TOF/MS system was performed to identify the serum differential metabolites between the NASH and control groups. Results: The liver weight was increased in the NASH group, accompanied by significantly higher levels of serum TC, TG, ALT, AST, LDL-C, and lower HDL-C. HE, Masson, and oil red O staining showed the hepatocyte structure destroyed, lipid droplets accumulated, and fibers proliferated in the NASH group. Furthermore, 63 differential metabolites were identified by metabolomic analysis. Lipids and fatty acids were significantly up-regulated in the NASH group. The top 9 differential metabolites included cholesterol, methyl phosphate, taurine, alpha-tocopherol, aspartic acid, etc. Metabolites were mainly involved in amino acid metabolism (glycine, cysteine, taurine), spermine, fatty acid biosynthesis, urea cycle, bile acid metabolism pathways, etc. Conclusion: Metabonomics analysis identified 63 differential metabolites in the serum of NASH hamsters; among them, lipids and fatty acids had a key role and may be used as biomarkers for the early diagnosis of NASH. other: None.