Dickensjohansson6886

The aim of this study was to investigate the role of long non-coding Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1) in bladder cancer (BCa), and the mechanism of OIP5-AS1/microRNA-217 (miR-217)/metadherin (MTDH) in promoting the progression of BCa.

OIP5-AS1, miR-217 and MTDH expressions in BCa tissues and cells were detected by qRT-PCR or Western blot. CCK-8 and transwell assays were used to determine the proliferation and invasion of BCa cells. The correlation between OIP5-AS1 and miR-217, miR-217 and MTDH, and OIP5-AS1 and MTDH were studied by Luciferase reporter assay and Spearman correlation analysis. Statistical analysis of test data was performed using t-test.

OIP5-AS1 was upregulated in BCa tissues and cells, and OIP5-AS1 knockdown could inhibit the proliferation and invasion of BCa cells. MiR-217 was a direct-acting target of OIP5-AS1, and MTDH was a target of miR-217. OIP5-AS1 knockdown inhibits human BCa cell proliferation and invasion through miR-217/MTDH axis.

This study systematically explored the effect of OIP5-AS1 in human BCa. ICI 46474 MiR-217/MTDH pathway mediated the promotion of OIP5-AS1 in BCa cells proliferation and invasion. OIP5-AS1, as an oncogene, could be used as a biomarker for the treatment of BCa.

This study systematically explored the effect of OIP5-AS1 in human BCa. MiR-217/MTDH pathway mediated the promotion of OIP5-AS1 in BCa cells proliferation and invasion. OIP5-AS1, as an oncogene, could be used as a biomarker for the treatment of BCa.

The long non-coding RNA MIR503 host gene (MIR503HG) plays a role in suppressing or promoting cancer in many types of human malignant tumors. The role of MIR503HG in cervical cancer is still unknown.

The expression level of MIR503HG in cervical cancer tissues and cell lines was accessed using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay. The Cell Counting Kit-8 (CCK-8) assay and flow cytometric analysis were performed to assess cell proliferation and apoptosis in cervical cancer. The nude mouse xenograft experiment was used to examine the ability of MIR503HG in tumor formation. In our study, we found that the expression of MIR503HG was significantly reduced in cervical cancer tissues and cell lines. In vitro studies have shown that MIR503HG inhibited cell proliferation and invasion, and enhanced cell apoptosis in cervical cancer through the miR-191/CEBPB axis. MIR503HG regulated the expression of miR-191 via directly binding to miR-191.

The expression of MIR503HG had a negative correlation with miR-191 expression in cervical cancer tissues. MiR-191 regulated the expression of CEBPB by directly targeting 3'-UTR of CEBPB mRNA. Overexpression of MIR503HG inhibited cell proliferation, invasion and apoptosis in vitro, and inhibited tumor growth in vivo.

MIR503HG plays a role in suppressing tumors in cervical cancer and is a long-term non-coding RNA.

MIR503HG plays a role in suppressing tumors in cervical cancer and is a long-term non-coding RNA.

To investigate the mechanism by which LINC00958 affects osteosarcoma progression through miR-4306/CEMIP axis.

The microarray data (GSE66673) for gene expression in osteosarcoma cells were obtained from the Gene Expression Omnibus (GEO) database, and differentially expressed genes were analyzed by bioinformatics tools. Real-time quantitative PCR (RT-qPCR) was performed to detect the expression levels of LINC00958, miR-4306, and CEMIP in osteosarcoma tissues and cell lines. Western blot was performed to detect the expression levels of CEMIP. Subcellular fractionation analysis and RNA Fluorescence in situ hybridization (FISH) assay were performed to analyze the subcellular localization of LINC00958. The target relationship between LINC00958, CEMIP, and miR-4306 was verified by public bioinformatics database and dual-luciferase reporter assay. RNA immunoprecipitation (RIP) assay was performed to detect LINC00958 and miR-4306 bound to AGO2. The biological functions of LINC00958 and miR-205 on proliferation, ced proliferation, cell cycle, metastasis, and invasion of osteosarcoma cells while inducing cellular apoptosis. The introduction of miR-4306 inhibitors reversed the tumor-suppressing effect of silencing LINC00958. miR-4306 binds to CEMIP and suppressed its expression. Xenograft tumor experiments and tumor metastasis assays in nude mice demonstrated that silencing LINC00958 inhibited osteosarcoma cells' growth and metastasis while inhibiting miR-4306 reversed this effect. Kaplan-Meier analysis showed that high expression of LINC00958 was significantly associated with poor prognosis of osteosarcoma patients.

LINC0095 promotes tumorigenesis and metastasis in osteosarcoma by competitively inhibiting miR-4306 expression, leading to elevated expression of CEMIP.

LINC0095 promotes tumorigenesis and metastasis in osteosarcoma by competitively inhibiting miR-4306 expression, leading to elevated expression of CEMIP.

To evaluate the effectiveness of case-based learning (CBL) in medical students' education through meta-analysis.

PubMed, Cochrane Library, Elsevier and other databases were searched to find randomized controlled trials (RCTs) of CBL teaching methods and other teaching methods published from January 1, 1995, to October 1, 2020. All included studies used the Cochrane risk bias assessment tool, and Review Manager software, version 5.3 (Copenhagen, Denmark), was used for the meta-analysis and systematic review.

A total of 8 studies were included with a total of 939 students, including 480 in the CBL group and 459 in the control group. Compared with other teaching methods, CBL teaching can improve medical students' academic performance (p=0.03) and case analysis ability (p<0.001).

CBL is an active teaching method that is effective for educating medical students and helps to improve their performance and case analysis ability.

CBL is an active teaching method that is effective for educating medical students and helps to improve their performance and case analysis ability.Naegleria fowleri is a deadly human pathogen that causes primary amoebic meningoencephalitis (PAM). In this study, in silico investigations of two important N. fowleri cathepsin B paralogs, i.e., copies of genes resulting from a gene duplication event, were carried out using comparative modeling and molecular dynamics (MD) simulations. Comparative models of both paralogs showed significant architectural similarity with their template, i.e., rat cathepsin B. However, in N. fowleri cathepsin B (UniProt ID X5D761) and putative cathepsin B (UniProt ID M1HE19) enzymes, eleven and fifteen residues in the occluding loop regions were deleted, respectively, suggesting that these enzymes have a short occluding loop. Thus, it is concluded that N. fowleri cathepsin B and putative cathepsin B enzymes lack exopeptidase activity but possess enhanced endopeptidase activity and an affinity for macromolecular inhibitors. MD simulations further confirmed that prosegments (macromolecular inhibitors) bond more tightly with both enzymes than with wild-type cathepsin B.