Objective To investigate the biological function and potential mechanisms of long non-coding RNA(lncRNA)neurensin 2-antisense RNA 1(NRSN2-AS1)in liver cancer cells.Methods The Encyclopedia of RNA Interactomes(ENCORI)database was used to analyze the expression levels of NRSN2-AS1 in liver cancer tissues and normal tissues as well as its association with the prognosis of patients.Stable lncRNA NRSN2-AS1 cell lines,overexpressed or knockdown,were constructed.The effects of NRSN2-AS1 on tumor cell proliferation were explored using CCK-8 and colony formation assays.Transwell and wound healing assays were employed to examine the role of NRSN2-AS1 in tumor cell migration and invasion.The impact of NRSN2-AS1 on tumor cell aerobic glycolysis was assessed by measuring hexokinase activity,glucose uptake,ATP and etracellular lactate levels.Quantitative real-time PCR(qPCR)and Western blotting were used to evaluate the effects of NRSN2-AS1 on the mRNA and protein expression levels of hexokinase 2(HK2)in tumor cells.Results Analysis from the ENCORI database revealed that NRSN2-AS1 was upregulated in liver cancer tissues compared to normal tissues,and that high expressions of NRSN2-AS1 were closely associated with poor prognosis of patients.In vitro functional assays demonstrated that overexpression of NRSN2-AS1 promoted proliferation,migration,and invasion of liver cancer cells,and enhanced glycolysis levels while knockdown of NRSN2-AS1 inhibited these processes and suppressed glycolysis.Furthermore,overexpression of NRSN2-AS1 increased the mRNA and protein levels of HK2 while knockdown of NRSN2-AS1 decreased HK2 expression in liver cancer cells.Conclusion NRSN2-AS1 is highly expressed in liver cancer tissues,and it may promote liver cancer progression by enhancing HK2 expression and aerobic glycolysis.

The management of antibiotic-resistant, bacterial biofilm infections in skin wounds poses an increasingly challenging clinical scenario. Pseudomonas aeruginosa infection is difficult to eradicate because of biofilm formation and antibiotic resistance. In this study, we identified a new benzothiazole derivative compound, SN12 (IC₅₀ = 43.3 nmol/L), demonstrating remarkable biofilm inhibition at nanomolar concentrations in vitro. In further activity assays and mechanistic studies, we formulated an unconventional strategy for combating P. aeruginosa-derived infections by targeting the two-component (Gac/Rsm) system. Furthermore, SN12 slowed the development of ciprofloxacin and tobramycin resistance. By using murine skin wound infection models, we observed that SN12 significantly augmented the antibacterial effects of three widely used antibiotics-tobramycin (100-fold), vancomycin (200-fold), and ciprofloxacin (1000-fold)-compared with single-dose antibiotic treatments for P. aeruginosa infection in vivo. The findings of this study suggest the potential of SN12 as a promising antibacterial synergist, highlighting the effectiveness of targeting the two-component system in treating challenging bacterial biofilm infections in humans.

Objective: To analyze the expression and clinical prognostic significance of nuclear Dbf2-related kinase 1 ( NDR1 ) in hepatocellular carcinoma ，and to investigate the biological function and regulatory mechanism of NDR1 in hepatocellular carcinoma cells． Methods: ENCORI database was used to analyze the correlation of NDR1 and c-Myc．Cycloheximide ( CHX) experiment analyzed the relationship between NDR1 and c-Myc protein stability．The expression levels of NDR1 in liver cancer tissues and normal tissues and its relationship with the survival rate of liver cancer patients were analyzed using the ENCORI database．MYC-NDR1 eukaryotic expression vector was constructed，transfected with hepatocellular carcinoma HepG2 cells，and its expression was verified by protein immuno blotting (Western blot) ; cell proliferation and migration ability were detected by CCK-8 assay，cell clone formation assay and scratch assay，respectively．The correlation between NDR1 and c-Myc expression was analyzed using the ENCORI database，and the relationship between NDR1 and c-Myc protein was investigated using a protein synthesis inhibitor CHX dosing assay. Results: The results of the ENCORI database showed that the expression of NDR1 in liver cancer tissues was higher than that in normal tissues and the overall survival rate of patients with high NDR1 expression was lower than that of patients with low NDR1 expression，and the difference was statistically significant (P＜0. 001) ．The results of the CCK-8 assay showed that the MYC-NDR1 group grew faster than the empty vector group (P＜0. 001) ．The clone formation assay showed that the number of clones in the MYC-NDR1 group was higher than that in the empty vector group (P＜0. 001) ．The cell scratch assay showed that the mean migration distance in the MYC-NDR1 group was greater than that in the empty vector group (P＜0. 001) ．ENCORI database analysis showed that NDR1 correlated with c-Myc expression (R = 0. 184，P＜0. 001) ; CHX dosing assay showed that the reduction of c-Myc protein in the MYC-NDR1 group was lower than that in the empty vector group during the same time． Conclusion NDR1 is highly expressed in hepatocellular carcinoma tissues，closely correlated with poor prognosis of hepatocellular carcinoma patients ，and positively correlated with the expression of c-Myc gene. The study successfully constructes MYC-NDR1 eukaryotic expression vector ，and the expression product MYC- NDR1 can increase the stability of c-Myc protein and promote the proliferation and migration of human hepatocellu- lar carcinoma cells.