LncRNA PCAT7 promotes non-small cell lung cancer progression by activating miR-486-5p/CDK4 axis-mediated cell cycle.

OBJECTIVE: Lung cancer remains one of the common cancers worldwide. Both LncRNA PCAT7 and miR-486-5p are tightly correlated with NSCLC. However, the relationship between PCAT7 and miR-486-5p and the detailed mechanisms underlying the effect of PCAT7 on NSCLC are not discovered yet. METHODS: GEPIA and ENCORI databases were used to determine the expression of PCAT7 in different cancers. CCK8, colony formation and Transwell assay were used to confirm the ability of cells. Luciferase reporter gene assay was employed to estimate the luciferase activity of the gene. Flow cytometry was used to compare cell cycle of NSCLC cells after indicated treatment. RESULTS: GEPIA combined ENCORI database illustrated that LncRNA PCAT7 was upregulated dramatically in NSCLC. The mRNA level of PCAT7 cells was higher than that in normal cells. Silencing PCAT7 inhibited the progression of NSCLC cells significantly. Data from ENCORI website showed that miR-486-5p was the target of PCAT7 and was negatively controlled by it. The data also showed that CDK4 could be bound and negatively regulated by miR-486-5p. MiR-486-5p inhibitor or CDK4 could partly restore the inhibitory effect of PCAT7 in NSCLC cells. In addition, silencing PCAT7 could arrest cell cycle to S in addition to G2 stage while transfecting miR-486-5p inhibitor or CDK4 could partially eliminate the retarding effects. CONCLUSION: In our study, we elaborated that LncRNA PCAT7 could promote the development of NSCLC cells by accelerating cell cycle via miR-486-5p/CDK4 axis.

Relationship between water quality, heavy metals and antibiotic resistance genes among three freshwater lakes.

Urban recreational lakes are impacted by consistent anthropogenic activities and are significant sources of heavy metals and antibiotic resistance genes (ARGs). In this study, three urban lakes of varying size and anthropogenic impact in Nanjing, China, were investigated for the abundance of ten ARGs, six physicochemical factors and four heavy metals. Correlations between heavy metals and physicochemical parameters against ARGs were performed to investigate the presence of ARGs in the lakes. The water quality data indicated that the lakes were on par with levels 3 and 4 of the Chinese surface water environmental standards, signifying disturbing pollution levels in the lakes. The lakes were dominant with high amounts of sul1, sul2 and strA genes, and the sum of these three genes appropriated over 38.9-84.4% in all three lakes, while the sum of tetM, tetQ and ermB genes occupied a minor proportion (0.1-1.4%). High levels of vancomycin resistance genes were found in the three lakes. Spearman analysis indicated that Chlα, cadmium, lead and copper had a significant positive correlation with sul2 and strB. The results of redundancy analysis displayed that Chlα and co-selection with certain heavy metals were the major factors driving the propagation of specific genes in three lakes. We believe our study contributes by adding further knowledge to existing antibiotic resistance gene abundance studies in recreational urban lakes with significant anthropogenic impacts.

Allicin Improves Lung Injury Induced by Sepsis via Regulation of the Toll-Like Receptor 4 (TLR4)/Myeloid Differentiation Primary Response 88 (MYD88)/Nuclear Factor kappa B (NF-κB) Pathway.

BACKGROUND The aim of this study was to assess the effects and mechanisms of allicin in a sepsis-induced lung injury in vivo study. MATERIAL AND METHODS The rats (n=54) were divided into 6 groups: Normal, DMSO, LPS, LPS+LD, LPS+MD, and LPS+HD groups. After being treated by different methods, we collected the lung tissues of different groups and evaluated the pathology by HE staining and positive apoptosis cells by TUNEL. We assessed the W/D ratio, inflammatory cytokines (TNF-alpha, IL-6 and IL-1ß), and relative protein expressions (TLR4, MyD88, NF-kappaB, caspase-3, and caspase-9) by IHC assay. RESULTS Compared with LPS group, the lung injury and positive cell number of allicin treated groups were significantly improved with dose-dependent (P<0.05, respectively) and the W/D ratio and TNF-alpha, IL-6 and IL-1ß concentration were significantly down-regulation compared with those of LPS group with dose-dependent (P<0.05, respectively). By IHC, the TLR4, MyD88, NF-kappaB, caspase-3 and caspase-9 protein activities of allicin treated groups were significantly suppressed compared with those of LPS group (P<0.05, respectively) in lung tissues. CONCLUSIONS This in vivo study shows that allicin improved sepsis-induced lung injury by regulation of TLR4/MyD88/NF-kappaB.