Data_Sheet_1_LncRNA RP11-499E18.1 Inhibits Proliferation, Migration, and Epithelial–Mesenchymal Transition Process of Ovarian Cancer Cells by Dissociating PAK2–SOX2 Interaction.XLSX

Background: Ovarian cancer (OC)is a deadly gynecological malignancy worldwide. It is urgent to identify diagnostic biomarkers of OC to disclose the underlying mechanism.Methods and Materials: Bioinformatics analysis was used to identify target genes. Gene expression was detected and altered by qRT-PCR and cell transfection, respectively. The interaction between RP11-499E18.1 and PAK2, as well as that between PAK2 and SOX2, was determined using RNA pulldown, RNA immunoprecipitation (RIP), and co-immunoprecipitation (co-IP) assay, respectively. Localizations of RP11-499E18.1, PAK2, and SOX2 were respectively determined employing immunohistochemical (IHC), IF, and FISH. The regulatory effects of RP11-499E18.1, PAK2, and SOX2 on OC cell proliferation, migration, colony formation, epithelial–mesenchymal transition (EMT)-related factor expression, and SOX2 nuclear translocation were determined. Finally, the effects of RP11-499E18.1 and PAK2 expression on the tumor growth in nude mice were determined.Results: RP11-499E18.1, PAK2, and SOX2 were selected in our study. RP11-499E18.1 was downregulated, while PAK2 and SOX2 was upregulated in OC tissues and cells. RP11-499E18.1 coexists in the nucleus and cytoplasm of OC cells. There is an interaction between RP11-499E18.1 and PAK2, as well as PAK2 and SOX2 in OC cells. Alteration of RP11-499E18.1 and PAK2 expression both had no influence on PAK2 and SOX2 levels, but PAK2 upregulation notably augmented p-SOX2 level. RP11-499E18.1 overexpression suppressed OC cell proliferation, migration, and colony formation, as well as SOX2 nuclear translocation. Besides, it inhibited tumor growth in nude mice. However, these effects were notably reversed by PAK2 upregulation and eventually offset by SOX2 knockdown. Additionally, RP11-499E18.1 overexpression reduced PAK2–SOX2 interaction and SOX phosphorylation, and increased the binding of RP11-499E18.1 by PAK2.Conclusion: These lines of evidence demonstrated that RP11-499E18.1 might play its tumor suppressor roles in OC via regulation of the RP11-499E18.1–PAK2–SOX2 axis. This research indicated that RP11-499E18.1 might be used as a diagnostic biomarker for OC in the future.</p

Data_Sheet_2_LncRNA RP11-499E18.1 Inhibits Proliferation, Migration, and Epithelial–Mesenchymal Transition Process of Ovarian Cancer Cells by Dissociating PAK2–SOX2 Interaction.DOCX

Background: Ovarian cancer (OC)is a deadly gynecological malignancy worldwide. It is urgent to identify diagnostic biomarkers of OC to disclose the underlying mechanism.Methods and Materials: Bioinformatics analysis was used to identify target genes. Gene expression was detected and altered by qRT-PCR and cell transfection, respectively. The interaction between RP11-499E18.1 and PAK2, as well as that between PAK2 and SOX2, was determined using RNA pulldown, RNA immunoprecipitation (RIP), and co-immunoprecipitation (co-IP) assay, respectively. Localizations of RP11-499E18.1, PAK2, and SOX2 were respectively determined employing immunohistochemical (IHC), IF, and FISH. The regulatory effects of RP11-499E18.1, PAK2, and SOX2 on OC cell proliferation, migration, colony formation, epithelial–mesenchymal transition (EMT)-related factor expression, and SOX2 nuclear translocation were determined. Finally, the effects of RP11-499E18.1 and PAK2 expression on the tumor growth in nude mice were determined.Results: RP11-499E18.1, PAK2, and SOX2 were selected in our study. RP11-499E18.1 was downregulated, while PAK2 and SOX2 was upregulated in OC tissues and cells. RP11-499E18.1 coexists in the nucleus and cytoplasm of OC cells. There is an interaction between RP11-499E18.1 and PAK2, as well as PAK2 and SOX2 in OC cells. Alteration of RP11-499E18.1 and PAK2 expression both had no influence on PAK2 and SOX2 levels, but PAK2 upregulation notably augmented p-SOX2 level. RP11-499E18.1 overexpression suppressed OC cell proliferation, migration, and colony formation, as well as SOX2 nuclear translocation. Besides, it inhibited tumor growth in nude mice. However, these effects were notably reversed by PAK2 upregulation and eventually offset by SOX2 knockdown. Additionally, RP11-499E18.1 overexpression reduced PAK2–SOX2 interaction and SOX phosphorylation, and increased the binding of RP11-499E18.1 by PAK2.Conclusion: These lines of evidence demonstrated that RP11-499E18.1 might play its tumor suppressor roles in OC via regulation of the RP11-499E18.1–PAK2–SOX2 axis. This research indicated that RP11-499E18.1 might be used as a diagnostic biomarker for OC in the future.</p

The application of N-butyl Phosphorothioate Triamine and Dicyandiamide changes the soil N₂O production path

This study aims to explore the effect of nitrification inhibitor combined with urease inhibitor on soil N2O emission under different nitrogen application depths. We carried out a soil column simulation test under 25°C. The combination of 1% N-butyl Phosphorothioate Triamine (NBPT) and 5% Dicyandiamide (DCD) was added to the soil. Anaerobically digested pig slurry (ADPS) was used as a nitrogen source and applied to four soil depths (soil surface (0 cm), 5 cm, 10 cm, and 15 cm, respectively). It was found that the inhibitory effects of NBPT and DCD on the soil N2O emission were significantly affected by different nitrogen application depths. When the ADPS was applied at 15 cm, 10 cm, and on the soil surface, the combination of 1% NBPT and 5% DCD could inhibit soil N2O emission by 46.1%, 21.7%, and 34.6%, respectively. Redundancy analysis (RDA) showed that the addition of inhibitors changed the microbial paths of soil N2O production. The dominant microbial path of soil N2O production after adding inhibitors was from ammonia oxidation dominated by AOB-amoA to denitrification dominated by nirS and nirK.</p

Synergistic Effects of Initial Moisture Content and Particle Size on Drying Rate and Heat Production during Bio-Drying of Sludge after Electro-Dewatering

Electro-dewatered sludge (EDS) can be bio-dried alone, instead of adding bulking agents. The initial moisture content (IMC) and particle size of the electro-dewatered sludge affect the efficiency and energy consumption during the bio-drying process. This study aimed to investigate the synergistic effects of sludge IMC and particle size on the drying rate and heat production of bio-drying with EDS. Experiments were conducted with two different IMC sludge and two different sludge particle sizes. Results showed that the highest moisture removal rate was 43.18% in treatment T4, which had materials with a smaller particle size (<3 mm) and lower IMC (38.69%). And bio-drying of T4 had the highest biological heat production (7413.14 kJ, i.e., 741.31 kJ/kg sludge), and the lowest bio-drying index (the ratio of water loss to volatile solid loss) was 7.10 among the four treatments. Five thin-layer drying kinetic models and a nonlinear regression method were analyzed to estimate the bio-drying kinetic parameters. The Midilli et al. model had a better fitting result, and the highest R2 value was 0.9929 during bio-drying of EDS. The new coefficients k (0.1465) and n (1.0898) were obtained. Through the heat balance, the heat used for evaporation was 40–57% of the total energy consumption (5873–9140 kJ). According to the PCA, the particle size had a great influence on the bio-drying process. Also, the particle size positively correlated with temperature, moisture ratio, and drying rate

Data_Sheet_1_Exploring antibiotic resistance load in paddy-upland rotation fields amended with commercial organic and chemical/slow release fertilizer.docx

Agricultural fertilization caused the dissemination of antibiotic resistance genes (ARGs) in agro-ecological environment, which poses a global threat to crop-food safety and human health. However, few studies are known about the influence of different agricultural fertilization modes on antibiotic resistome in the paddy-upland rotation soils. Therefore, we conducted a field experiment to compare the effect of different fertilization (chemical fertilizer, slow release fertilizer and commercial organic fertilizer replacement at various rates) on soil antibiotic resistome in paddy-upland rotation fields. Results revealed that a total of 100 ARG subtypes and 9 mobile genetic elements (MGEs) occurred in paddy-upland rotation soil, among which MDR-ARGs, MLSB-ARGs and tet-ARGs were the dominant resistance determinants. Long-term agricultural fertilization remarkably facilitated the vertical accumulation of ARGs, in particular that blaampC and tetO in relative abundance showed significant enrichment with increasing depth. It’s worth noting that slow release fertilizer significantly increased soil ARGs, when comparable to manure with 20% replacing amount, but chemical fertilizer had only slight impact on soil ARGs. Fertilization modes affected soil microbial communities, mainly concentrated in the surface layer, while the proportion of Proteobacteria with the highest abundance decreased gradually with increasing depth. Furthermore, microbial community and MGEs were further proved to be essential factors in regulating the variability of ARGs of different fertilization modes by structural equation model, and had strong direct influence (λ = 0.61, p < 0.05; λ = 0. 55, p < 0.01). The results provided scientific guidance for reducing the spreading risk of ARGs and control ARG dissemination in agricultural fertilization.</p

Green and Efficient Al-Doped LaFe_<i>x</i>Al_1–<i>x</i>O₃ Perovskite Oxide for Enhanced Phosphate Adsorption with Creation of Oxygen Vacancies

La-based metal oxide materials are environmentally friendly and show promise for phosphate adsorption. A series of Al-doped perovskite oxides, such as LaFexAl1–xO3, were prepared using a facile citric acid-assisted sol–gel method. The characterization results demonstrated that with optimized Al doping, there was a significant increase in the specific surface area and increased defect content of perovskite oxide LaFexAl1–xO3. Adsorption experiments showed that the performance of phosphate removal by LaFexAl1–xO3 was largely enhanced due to the improved adsorption capacity, which is maximum eight times higher compared with control perovskites prepared under neutral conditions. The mass transfer rate for adsorption was considerably boosted with phosphate removal within the initial 15 min. Spectroscopy analysis and density functional theory calculation results showed that the process of phosphate removal by the Al-doped perovskite oxides LaFexAl1–xO3 involved electrostatic interactions, an inner-sphere complex, and surface oxygen vacancies, among which the creation of oxygen vacancies caused by the Al doping was the predominant mechanism for reducing the bonding barrier during adsorption and generating adsorption sites. The results enable the development of a green and efficient perovskite adsorbent with a La-based perovskite material for phosphorus removal

Additional file 2 of Transcription factor AP2 enhances malignancy of non-small cell lung cancer through upregulation of USP22 gene expression

Additional file 1. Supplementary figures and tables

MOESM2 of Ubiquitin-specific protease 22 is critical to in vivo angiogenesis, growth and metastasis of non-small cell lung cancer

Additional file 2. Differentially expressed gene list in USP22-Ko A549 and H1299 cells

MOESM1 of Ubiquitin-specific protease 22 is critical to in vivo angiogenesis, growth and metastasis of non-small cell lung cancer

Additional file 1 Fig. S1. Differentially expressed gene in USP22-Ko A549 and H1299 cells. Fig. S2. Impact of knockdown of USP22 on H2Bub1/methylatiom of H3K4/K79, cancer cell proliferation, and cell cycle progression. Fig. S3. Negative USP22 IHC stains in adjacent normal cells and tissues. Figure 4. Impact of knockout of USP22 on in vitro migration and invasion of A549 and H1299 cells. Fig. S5. Elevated USP22 in cancer cells survived cisplatin treatment. Fig. S6. Dynamics of P53 in A549 and USP22-Ko cells after 5 and 10 Gy irradiation

Supplementary Figures S1-S6 from G9a Promotes Invasion and Metastasis of Non–Small Cell Lung Cancer through Enhancing Focal Adhesion Kinase Activation via NF-κB Signaling Pathway

Figure S1. G9a silencing suppressed cell proliferation in A549 and H1299 NSCLCs Figure S2. Cell migration and invasion was suppressed in NSCLCs treated by G9a inhibitor UNC0638 Figure S3. G9a overexpression increased cell proliferation in NSCLCs Figure S4. FAK inhibitor attenuates the enhanced cell migration and invasion by G9a overexpression Figure S5. knockdown of G9a suppressed tumor metastasis in vivo. Figure S6. NF-kappa;B signaling pathway is independent of Wnt signaling pathway.</p