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The critical roles of N6-methyladenosine (m6A) modification have been demonstrated by more and more evidence. However, the cross talk of m6A and long noncoding RNAs (lncRNAs) in non-small cell lung cancer (NSCLC) tumorigenesis is still unclear. Here, this work focused on the functions and molecular mechanism of m6A-modified lncRNA DLGAP1 antisense RNA 2 (DLGAP1-AS2) in NSCLC. Microarray analysis found that lncRNA DLGAP1-AS2 is upregulated in NSCLC cells. Clinical data showed that DLGAP1-AS2 high-expression was correlated with advanced pathological stage and poor prognosis. Functionally, DLGAP1-AS2 overexpression promoted the aerobic glycolysis and DLGAP1-AS2 knockdown suppressed the tumor growth of NSCLC cells. Mechanistically, m6A methyltransferase METTL3 enhanced the stability of DLGAP1-AS2 via m6A site binding. Moreover, DLGAP1-AS2 interacted with YTHDF1 to enhance the stability of c-Myc mRNA through DLGAP1-AS2/YTHDF1/m6A/c-Myc mRNA. In conclusion, our work indicates the functions of m6A-modified DLGAP1-AS2 in the NSCLC aerobic glycolysis, disclosing a potential m6A-dependent manner for NSCLC treatment. [ABSTRACT FROM AUTHOR]

Context: Non-alcoholic fatty liver disease (NAFLD), the most common chronic liver disease, can develop into metabolic associated fatty liver disease (MAFLD). Gypenosides (GP), the main phytochemical component of Gynostemma pentaphylla (Thunb.) Makino (Cucurbitaceae), have been applied for treatment of metabolic diseases. Objective: We investigate how GP modulate MAFLD-related hepatic steatosis and intestinal barrier injury. Materials and methods: In cell experiments, Caco-2 cells were treated with GP (150 or 200 lmol/L, 24 h), following lipopolysaccharide (LPS) exposure (10 lg/mL, 24 h) to mimic MAFLD in vitro. In in vivo experiments, control, model and modelþGP groups were set. High fructose diet/high fat (HFD/HF)-fed (12 weeks) MAFLD rats received GP treatment (300mg/kg, 6 weeks), followed by intra-peritoneal glucose tolerance test and histopathological examination of rat liver and intestinal mucosa using haematoxylin-eosin staining. Results: GP at 200 lM significantly reversed LPS-induced decreases in transepithelial electrical resistance (TER) value (25%), protein expression of occludin (two fold) and ZO-1 (four fold), and the ratio of p-AMPK to AMPK (five fold), while partially repressing LPS-induced leakage of FD4 (50%) and LPS-induced increases in the Toll-like receptor 4 (TLR4) level (50%) and the ratio of p-p65 to p65 (55%). Compared with the model rats, rats with GP treatment presented a reduction in gain of weight and glucose tolerance. In addition, GP alleviated HFD/HF-induced histopathological abnormalities in rat liver and intestinal mucosa. Conclusions: GP attenuates hepatic steatosis and intestinal barrier injury in MAFLD rats via the AMPK and TLR4/nuclear factor kappa B (NF-jB) pathways, providing a potential treatment for MAFLD patients. [ABSTRACT FROM AUTHOR]

Comaster schlegelii, belonging to the family Comatulidae, is a variable feather star distributed in the Pacific Ocean. The complete mitochondrial genome of this species was 15,887 bp in length, consisting of 13 protein-coding genes, 22 transport RNA genes, two ribosomal RNA genes and one control region. The whole mitochondrial genome of C. schlegelii had a high AT content of 72.73%. The phylogenetic relationship was reconstructed with 16 relevant echinoderms, which revealed C. schlegelii was closely clustered with Anneissia pinguis in the family Comatulidae. [ABSTRACT FROM AUTHOR]