Active dissolved organic nitrogen cycling hidden in large river and environmental implications.

Large rivers are important terrestrial dissolved organic matter (DOM) sources to marginal seas, and dissolved organic nitrogen (DON) plays an essential role in DOM cycling. The Yellow River ranks as the fifth largest river (in length) in the world and is well-known for its high dissolved inorganic nitrogen (DIN) concentration and relatively low DON concentration, leading to extreme measuring uncertainties in DON and nitrogen isotopic composition (δ15N), consequently leaving its DON cycling as an unresolved puzzle. To fill such a knowledge gap, we analyzed 17 samples from the middle to downstream with a combination of spectroscopy, tangential flow filtration, nitrogen isotope, and DNA sequencing. DON<1kDa dominated the DON pool and significantly correlated inversely with DIN, indicating the DON<1kDa mineralized into nitrate. This finding was further supported by the observed Rayleigh fractionation in δ15NDON<1kDa and the spatial distribution pattern of ammonia-oxidizing bacteria/archaea abundance. The redundancy analysis revealed that the geographical features and the microbial community were closely related, which joined together to drive the DON cycling. In addition, we propose a rational method to quantify the flux of mineralized DON in large rivers. This study discovered the active DON cycling hidden in high DIN large river and highlighted the importance of DON mineralization as well as its role in marginal seas carbon cycling.

Integrated effects of Ulva prolifera bloom and decay on nutrients inventory and cycling in marginal sea of China.

Ulva prolifera blooms occur annually in the Yellow Sea. Most studies focus on how U. prolifera blooming is influenced by nitrogen chemical forms and concentrations, while little concern goes to how U. prolifera bloom-decay cycle would impact local seawater nutrients structure. Therefore, we use 15N-labeled NO3 tracers and transcriptome analysis to determine N uptake, metabolism, and interconversion during U. prolifera growth and decay, so that we can quantify the conversions rate and fluxes of different nitrogen chemical forms. U. prolifera absorbes 17.37 µmol g-1·d-1 NO3-N during growth. NO3-N predominates (73.75-92.15%) in the dissolved inorganic nitrogen (DIN) in U. prolifera. During decay, NH4-N accountes for 60.87-92.13% of the in-cell DIN. The decomposing U. prolifera releases considerable amounts of NH4-N and dissolved organic nitrogen (DON) (63.8-98.2% < 1 kDa fraction and 1.8-36.2% is > 1 kDa fraction) into the ambient environment. The high DON release rate (59.57 µmol g-1 d-1) indicates active DON biosynthesis in U. prolifera. The isotope 15NO3-N tracer showes that 73.6% of the 15NO3-N is transformed to DON. The <1 kDa and the >1 kDa fractions account for 67.46-90.86% and 9.14-32.54% of the DON, respectively. The high efficiency of U. prolifera in utilizing NO3-N is explained by the responsive nitrate/nitrite transporter in cell membrane, and the DON biosynthesized capability is attributed to the up-regulated glutamine synthetase. Our study highlights the unique role of U. prolifera as a "Nitrogen-Pump" in converting nitrogen chemical forms during its bloom-decay cycle and quantifies its impacts on local N-nutrients inventory.

Long non-coding RNA MALAT1 regulates oxaliplatin-resistance via miR-324-3p/ADAM17 axis in colorectal cancer cells.

BACKGROUND: Colorectal cancer (CRC) is one of the most general malignant tumors. Accumulating evidence implied that long non-coding RNA Metastasis Associated Lung Adenocarcinoma Transcript 1 (MALAT1) participated in the tumorigenesis of CRC. However, the effect of MALAT1 in drug-resistance needed to be further illustrated. METHODS: Levels of MALAT1, microRNA (miR)-324-3p, and a disintegrin and metalloprotease metallopeptidase domain 17 (ADAM17) were detected using quantitative real-time polymerase chain reaction (qRT-PCR) or western blot assay. Cell Counting Kit 8 (CCK-8) was used to assess the half maximal inhibitory concentration (IC50) of oxaliplatin (Ox). Meanwhile, cell proliferation, migration and apoptosis were detected by CCK-8, transwell assay, and flow cytometry, respectively. The interaction between miR-324-3p and MALAT1 or ADAM17 was clarified by dual-luciferase reporter assay. Also, the effect of MALAT1 on tumor growth was detected in xenograft tumor mice treated with Ox. RESULTS: Significant up regulation of MALAT1 and ADAM17, and decrease of miR-324-3p were observed in Ox-resistant CRC tissues and cells. MALAT1 deficiency enhanced the sensitivity of Ox-resistant CRC cells response to Ox, while miR-324-3p repression or ADAM17 acceleration could overturn this effect. Moreover, MALAT1 silencing repressed tumor growth in Ox-treated nude mice. Mechanically, MALAT1 exerted promotion effect on the resistance response to Ox via miR-324-3p/ADAM17 axis in Ox-resistant CRC cells. CONCLUSION: MALAT1 modulated the sensitivity of Ox through ADAM17 in Ox-resistant CRC cells by sponging miR-324-3p, thus MALAT1 might serve as a novel insight for the therapy of CRC.

Nitrate processing traced by nitrate dual isotopic composition in the early spring in the Changjiang (Yangtze River) Estuary and adjacent shelf areas.

Nitrate is the major chemical form of N-nutrient to sustain primary production in Changjiang Estuary and adjacent seawaters. We employed δ15N-NO3- and δ18O-NO3- to constrain the source, cycling, and sink of nitrate in early spring. Both δ15N-NO3- and δ18O-NO3- differentiate significantly among Changjiang Diluted Water (CDW), Yellow Sea Coastal Current (YSCC), and Taiwan Warm Current (TWC). In coastal areas, nitrate distribution and its isotopes are mainly affected by Changjiang inputs. Chemical fertilizers and sewage & manure originated nitrate jointly contribute the most nitrate in CDW. In offshore areas, nitrification contributes 44 ± 21% of the nitrate in YSCC and 17 ± 16% in TWC; assimilation is the dominant process to remove nitrate in TWC (35 ± 16%). Overall, nitrification and assimilation are the key nitrate cycling processes in early spring and co-shape the offshore distribution pattern of nitrate and its dual isotopes.

siRNA Targeting of the SNCG Gene Inhibits the Growth of Gastric Carcinoma SGC7901 Cells in vitro and in vivo by Downregulating the Phosphorylation of AKT/ERK.

The aim of the study was to evaluate the effects of synuclein-γ (SNCG) silencing on gastric cancer SGC7901 cells and to elucidate the associated mechanisms. pGCSIL-lentiviral siRNA targeting of the SNCG gene was employed to inhibit SNCG expression. Several experiments such as quantitative real-time PCR, Western blotting, MTT, colony formation, migration assay, and flow cytometry were performed to investigate the biological behavior of infected SGC7901 cells. BALB/c nude mice were used as tumor xenograft models to assess the effects of SNCG silencing on tumor growth. Western blot analysis was carried out to determine the relative levels of AKT, p-AKT, ERK, and p-ERK expression. Our results showed that SNCG was overexpressed in SGC7901 cells as compared to normal gastric mucosal epithelial cells. SGC7901 cells transfected with SNCG siRNA demonstrated significantly decreased gastric cancer growth (p < 0.01), reduced cell migration, cell cycle arrest in the G0/G1 phase, promoted tumor cell apoptosis (p < 0.01), and inhibited tumorigenesis in xenograft animal models. Western blot analysis indicated that the protein levels of p-AKT and p-ERK were much lower in the SNCG siRNA group than in the control groups. The results of the present study suggest that SNCG siRNA plays a significant role in the proliferation, migration, and tumorigenesis of gastric cancer by downregulating the phosphorylation of AKT and ERK. RNA interference-mediated silencing of SNCG may provide an opportunity to develop a novel treatment strategy for gastric cancer.