Proteins Denaturation By making use of Magnetic Molecularly Published Polymer bonded Nanoparticles

Results ASB16-AS1 expression was significantly elevated in OS tissues and cell lines, and increased ASB16-AS1 expression was related to patients' tumor size, TNM stage, and distant metastasis. The overall survival rate of OS patients presenting high ASB16-AS1 expression was shorter than that of patients presenting low ASB16-AS1 expression. Reduced ASB16-AS1 expression inhibited OS cell proliferation, migration, and invasion; promoted cell apoptosis; and impaired tumor growth in vivo. Mechanistically, ASB16-AS1 served as a sponge for miR-760 and positively modulated the expression of its target HDGF. Finally, inhibiting miR-760 and restoring HDGF expression abolished the impacts of ASB16-AS1 knockdown on the malignant characteristics of OS cells. Conclusion ASB16-AS1 is a novel oncogenic lncRNA in OS cells. ASB16-AS1 increased HDGF expression by sponging miR-760, thereby conferring cancer-promoting roles in OS. ASB16-AS1 is a potential early diagnostic and therapeutic target in OS. © 2020 Yin et al.Background Low-grade gliomas (LGG), approximately constitute one-third of all types of gliomas, are prone to relapse and metastasis. MicroRNA-138 (miR-138) is reported to be dysregulated in diverse human tumors and mainly function as a tumor suppressor. In this study, we analyzed the expression profile and function of miR-138 in LGG. Methods Quantitative PCR (qPCR) and public database bioinformatics analysis were performed to determine the miR-138 levels in LGG. MiR-138 overexpression in LGG cells was achieved by miR-138 mimics transfection. U18666A Cell proliferation was assessed by CCK8, EdU and colony formation assays. Cell invasion and migration were analyzed by transwell and wound-healing assays. Xenograft model was employed to study the role of miR-138 in LGG growth in vivo. The target of miR-138 was validated by multiple methods, such as luciferase reporter assay, RT-qPCR and Western blot. Bioinformatics analysis was conducted to explore the molecular mechanisms by which miR-138 contributed to LGG progression. Results miR-138 was significantly downregulated in LGG tumor tissues and low expression of miR-138 was significantly associated with poor prognosis as well as relapse and metastasis in LGG patients. Functional analysis indicated that ectopic miR-138 expression suppressed LGG cell growth and invasive phenotype in vitro, and inhibited tumor development in vivo. Moreover, miR-138 directly targeted and repressed insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) by targeting the 3'-UTR of IGF2BP2, inhibiting epithelial to mesenchymal transition (EMT) to attenuate LGG aggressiveness. In addition, we found that elevated IGF2BP2 expression correlates with poor survival of LGG patients. Conclusion miR-138 may function as a tumor inhibitor by directly inhibiting IGF2BP2 and suppressing EMT in the progression of LGG. © 2020 Yang et al.Background Mounting evidence has reported that microRNA-154-5p (miR-154-5p) is involved in the development of multiple cancers, but its function in nasopharyngeal carcinoma (NPC) remains not well investigated. Methods Real-time quantitative PCR (qRT-PCR) was used to detect miR-154-5p expression in NPC tissues and cells. CCK8, colony formation, wound healing and transwell assays were performed to assess cell proliferation, migration and invasion. Dual-luciferase reporter assays and Western blots were performed to confirm the target gene of miR-154-5p. Rescue experiments were conducted to explore the influence of target gene KIF14 on the functions of miR-154-5p. Xenograft tumor model was conducted to detect the effect of miR-154-5p in vivo. Results qRT-PCR results revealed that the expression of miR-154-5p was down-regulated in NPC tissues and cell lines compared to normal nasopharyngeal tissues and cell line. Overexpression of miR-154-5p inhibited cell migration and invasion. However, miR-154-5p had no influence on the proliferation of NPC cells. MiR-154-5p overexpression suppressed xenograft tumor metastasis in vivo. Dual-luciferase reporter analysis identified KIF14 as a target gene of miR-154-5p. Rescue experiments showed that knockdown of KIF14 reversed the effect of inhibiting miR-154-5p expression on NPC cell migration and invasion. Conclusion Taken together, miR-154-5p suppresses tumor migration and invasion by targeting KIF14 in NPC. The newly identified miR-154-5p/KIF14 interaction offers further insights into the progression of NPC, which may represent a novel target for NPC diagnosis and treatment. © 2020 Chen et al.Background Cisplatin (DDP) resistance has become an obstacle to chemotherapy for nasopharyngeal carcinoma (NPC) patients. Recent evidences indicate that long noncoding RNAs (lncRNAs) are involved in tumorigenesis and chemoresistance. However, the potential role of lncRNAs in NPC progression remains largely unknown. Methods First, lncRNA expression profiling in NPC was performed via microarray analysis. To explore the involvement of DLEU1 in DDP resistance, loss-of-function experiments were employed in vitro and in vivo. Bioinformatics analysis, luciferase reporter assay, qRT-PCR, and Western blot assays were used to investigate the underlying mechanisms. Results Here, we identified 153 differentially expressed lncRNAs. Among them, DLEU1 was remarkably up-regulated in NPC tissues and associated with worse outcome. Knock-down of DLEU1 could sensitize NPC cells to DDP in vitro and in vivo. Further investigations revealed that DLEU1 positively regulated BIRC6 expression via its competing endogenous RNA (ceRNA) activity on miR-381-3p. We also observed that BIRC6 overexpression or miR-381-3p silence could significantly reverse DLEU1-dependent DDP resistance. Conclusion Our data suggest that DLEU1 acts as an oncogene to promote DDP resistance and BIRC6 expression in NPC through interacting with miR-381-3p, which may help to develop new strategy against NPC chemoresistance. © 2020 Li et al.Purpose To determine levels of burnout among emergency medical services (EMS) professionals and the coping strategies they use to alleviate burnout and measure the association between burnout vs sociodemographic and work-related characteristics and coping strategies of EMS professionals. Methods This was a cross-sectional survey study conducted among 270 active-duty EMS professionals. The Maslach Burnout Inventory (MBI) - Health Services Survey was used to assess burnout. There are three scales of burnout depersonalization, emotional exhaustion, and personal achievement. Coping Methods Checklist (CMC) was used to assess coping strategies. Univariate descriptive statistics were used to explore sociodemographic characteristics of participants, level of burnout, and coping strategies. Primary bivariate analyses were used to determine variables significantly correlated with each of the three MBI scores. Multiple linear regression models were used to explore correlation between variables measured in the survey with each of the three MBI scales (emotional exhaustion, depersonalization, and personal accomplishment).