MiR-532-5p acts as a tumor suppressor and inhibits glioma cell proliferation by targeting CSF1.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "MiR-532-5p acts as a tumor suppressor and inhibits glioma cell proliferation by targeting CSF1, by Y.-P. Wang, J. Liu, D. Liu, X.-D. Wang, A.-M. Bian, D.-Z. Fang, X.-B. Hui, published in Eur Rev Med Pharmacol Sci 2019; 23 (20): 8964-8970-DOI: 10.26355/eurrev_201910_19295-PMID: 31696484" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19295.

Circ_0005075 stimulates the proliferation and metastasis of glioma via downregulating SIRT1.

OBJECTIVE: The aim of this study was to uncover the potential influence of circ_0005075 on the malignant progression of glioma and the underlying mechanism. PATIENTS AND METHODS: Circ_0005075 level in glioma tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The relation between circ_0005075 expression and metastasis of glioma patients was analyzed. Prognostic potential of circ_0005075 in glioma was assessed by calculating overall survival (OS) and progression-free survival (PFS). After knockdown or overexpression of circ_0005075, changes in the viability, migration, and wound closure percentage of T98-G and U87 cells were examined, respectively. Subsequently, expression pattern and prognostic value of SIRT1 in glioma patients were determined. Furthermore, the involvement of SIRT1 in glioma progression affected by circ_0005075 was evaluated through rescue experiments. RESULTS: Circ_0005075 was significantly up-regulated in glioma tissues and cell lines. Meanwhile, its expression level was significantly higher in glioma patients with lymphatic metastasis or distant metastasis when compared with those with negative metastasis. OS and PFS were both remarkably worse in glioma patients with high expression level of circ_0005075. Knockdown of circ_0005075 decreased the viability, migration, and wound closure percentage of T98-G cells. However, overexpression of circ_0005075 in U87 cells yielded the opposite trends. SIRT1 expression level was negatively regulated by circ_0005075 in glioma. QRT-PCR results demonstrated that SIRT1 was significantly down-regulated in glioma tissues and cell lines. High level of SIRT1 predicted better prognosis of glioma patients. Rescue experiments confirmed that SIRT1 was responsible for the regulatory role of circ_0005075 in the malignant progression of glioma. CONCLUSIONS: Circ_0005075 is up-regulated in glioma tissues and correlated with distant metastasis and poor prognosis of glioma patients. Furthermore, it aggravates the malignant progression of glioma by down-regulating SIRT1.

MiR-532-5p acts as a tumor suppressor and inhibits glioma cell proliferation by targeting CSF1.

OBJECTIVE: Recent studies have discovered a class of micro-RNAs (miRNAs), which are dysregulated in various tumors and associated with carcinogenesis. In our research, we aim to uncover the molecular functions of miR-532-5p in glioma development. PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was performed to detect miR-532-5p expression in 48 glioma samples and 4 glioma cell lines. The Pearson's Chi-square test was used to determine the association of miR-532-5p expression with several clinicopathological indexes in glioma patients. Besides, cell proliferation assay, colony formation assay, and Ethynyl deoxyuridine (EdU) incorporation assay were performed to explore in vitro effects of miR-532-5p on glioma cells. Furthermore, the interaction between miR-532-5p and CSF1 in glioma was studied by performing Western blot assay and Dual-Luciferase Reporter Gene Assay. RESULTS: Downregulated miR-532-5p expression was observed in glioma tissues compared with adjacent normal samples. MiR-532-5p expression was associated with the KPS score and tumor grading in glioma patients. Moreover, cell proliferation of glioma was inhibited after overexpression of miR-532-5p in vitro. Furthermore, CSF1 was a target of miR-532-5p in glioma. After overexpression of miR-532-5p, CSF1 was downregulated at mRNA and protein levels in vitro Besides, the expression of CSF1 in glioma tissues was negatively related to that of miR-532-5p. CONCLUSIONS: Malignant phenotypes of glioma cells were remarkably suppressed through the overexpression of miR-532-5p. MiR-532-5p/CSF1 axis was identified as a new therapeutic intervention for the treatment of glioma.

MicroRNA-129-3p suppresses tumor growth by targeting E2F5 in glioblastoma.

OBJECTIVE: Neuroma is the most common intracranial tumor. The mechanism of miRNA in glioma has gradually been understood. The purpose of this study was to investigate the role of MicroRNA-129-3p (miR-129-3p) in the pathogenesis of glioblastoma (GBM). PATIENTS AND METHODS: Differential expression of miR-129-3p in samples was analyzed by bioinformatics. PCR was used to detect the expression of miR-129-3p in samples. CCK8 assay was used to detect the cell viability. Transfection of mimic and inhibitor altered the expression of miR-129-3p, and the biological function of miRNA was explored. Luciferase reporter gene was used to detect target genes of miRNA. E2F5 expression was inhibited by transfection of small interfering RNAs. Western blotting was used to detect protein expressions of cells. RESULTS: miR-129-3p was low-expressed in the tissue samples. By transfecting mimic and the inhibitor, we found that increasing the expression of miR-129-3p can inhibit the cell viability. In contrast, inhibition of miR-129-3p promoted cell growth. Luciferase reporter gene and Western blot results suggested that E2F5 can be used as the target gene of miR-129-3p. Knockdown the target gene of the miR-129-3p, E2F5, also inhibited proliferation of glioblastoma. CONCLUSIONS: miR-129-3p can inhibit the growth of glioblastoma by down-regulating the expression of E2F5. miR-129-3p can be a new target for the treatment of glioblastoma. Our research provides new ideas for the target therapy of glioma.

Single nucleotide polymorphisms predisposing to asthma in children of Mauritian Indian and Chinese Han ethnicity.

Our objective was to investigate the distributions of six single nucleotide polymorphisms (SNPs) MS4A2 E237G, MS4A2 C-109T, ADRB2 R16G, IL4RA I75V, IL4 C-590T, and IL13 C1923T in Mauritian Indian and Chinese Han children with asthma. This case-control association study enrolled 382 unrelated Mauritian Indian children, 193 with asthma and 189 healthy controls, and 384 unrelated Chinese Han children, 192 with asthma and 192 healthy controls. The SNP loci were genotyped using polymerase chain reaction (PCR)-restriction fragment length polymorphism for the Chinese Han samples and TaqMan real-time quantitative PCR for the Mauritian Indian samples. In the Mauritian Indian children, there was a significant difference in the distribution of IL13 C1923T between the asthma and control groups (P=0.033). The frequency of IL13 C1923T T/T in the Mauritian Indian asthma group was significantly higher than in the control group [odds ratio (OR)=2.119, 95% confidence interval=1.048-4.285]. The Chinese Han children with asthma had significantly higher frequencies of MS4A2 C-109T T/T (OR=1.961, P=0.001) and ADRB2 R16G A/A (OR=2.575, P=0.000) than the control group. The IL13 C1923T locus predisposed to asthma in Mauritian Indian children, which represents an ethnic difference from the Chinese Han population. The MS4A2 C-109T T/T and ADRB2 R16G A/A genotypes were associated with asthma in the Chinese Han children.

Single nucleotide polymorphisms predisposing to asthma in children of Mauritian Indian and Chinese Han ethnicity

Our objective was to investigate the distributions of six single nucleotide polymorphisms (SNPs) MS4A2 E237G, MS4A2 C-109T, ADRB2 R16G, IL4RA I75V, IL4 C-590T, and IL13 C1923T in Mauritian Indian and Chinese Han children with asthma. This case-control association study enrolled 382 unrelated Mauritian Indian children, 193 with asthma and 189 healthy controls, and 384 unrelated Chinese Han children, 192 with asthma and 192 healthy controls. The SNP loci were genotyped using polymerase chain reaction (PCR)-restriction fragment length polymorphism for the Chinese Han samples and TaqMan real-time quantitative PCR for the Mauritian Indian samples. In the Mauritian Indian children, there was a significant difference in the distribution of IL13 C1923T between the asthma and control groups (P=0.033). The frequency of IL13 C1923T T/T in the Mauritian Indian asthma group was significantly higher than in the control group [odds ratio (OR)=2.119, 95% confidence interval=1.048-4.285]. The Chinese Han children with asthma had significantly higher frequencies of MS4A2 C-109T T/T (OR=1.961, P=0.001) and ADRB2 R16G A/A (OR=2.575, P=0.000) than the control group. The IL13 C1923T locus predisposed to asthma in Mauritian Indian children, which represents an ethnic difference from the Chinese Han population. The MS4A2 C-109T T/T and ADRB2 R16G A/A genotypes were associated with asthma in the Chinese Han children.

Ballistic and non-ballistic gas flow through ultrathin nanopores.

We show that ultrathin porous nanocrystalline silicon membranes exhibit gas permeance that is several orders of magnitude higher than other membranes. Using these membranes, gas flow obeying Knudsen diffusion has been studied in pores with lengths and diameters in the tens of nanometers regime. The components of the flow due to ballistic transport and transport after reflection from the pore walls were separated and quantified as a function of pore diameter. These results were obtained in pores made in silicon. We demonstrate that changing the pore interior to carbon leads to flow enhancement resulting from a change in the nature of molecule-pore wall interactions. This result confirms previously published flow enhancement results obtained in carbon nanotubes.

Prevalence of post-traumatic stress disorder among adolescents after the Wenchuan earthquake in China.

BACKGROUND: The Wenchuan earthquake was a catastrophic earthquake in China. The aim of this study is to explore longitudinally the rates of post-traumatic stress disorder (PTSD) and depression in adolescents after the Wenchuan earthquake, and to identify independent predictors of PTSD. METHOD: PTSD and depression symptoms among adolescents at 6, 12 and 18 months after the Wenchuan earthquake were investigated using the PTSD Checklist Civilian Version and the Beck Depression Inventory (BDI). Subjects in this study included 548 high school student survivors in a local boarding high school. RESULTS: The rates of PTSD symptoms were 9.7%, 1.3% and 1.6% at the 6-, 12- and 18-month follow-ups, respectively. BDI scores were found to be the best predictor of severity of PTSD at 6, 12 and 18 months. Gender was another variable contributing significantly to PTSD at 6 and 12 months after the earthquake. In the 12-month follow-up, home damage was found to be a predictor of severity of PTSD symptoms. Being a child with siblings was found to be a predictor of severity of PTSD symptoms at 12 and 18 months after the earthquake. CONCLUSIONS: PTSD symptoms changed gradually at various stages after the earthquake. Depression symptoms were predictive of PTSD symptoms in the 18-month follow-up study. Other predictors of PTSD symptoms included female gender and being a child with siblings. The results of this study may be helpful for further mental health interventions for adolescents after earthquakes.

Apolipoprotein A5 polymorphisms and risk of coronary artery disease: a meta-analysis.

The relation has not been reported consistently between the polymorphisms in the gene of apolipoprotein A5 (APO A5) and coronary artery disease (CAD). To clarify the discrepancy, we conducted a comprehensive search of PubMed and EMBASE for all available casecontrol studies to explore the association between two APO A5 polymorphisms and CAD. Two reviewers independently selected studies. Statistical analyses were carried out using the STATA software package v 10.0. Thirteen studies investigated the association between the APO A5 -1131T>C polymorphism and risk of CAD were selected in this meta-analysis with 5,050 cases and 7,272 controls. For the S19W APO A5 gene polymorphism, 5 studies were included with 2,196 cases and 3,933 controls. We observed a significant statistical association between Apo A5 -1131T>C polymorphism and CAD (recessive genetic model: OR = 1.73, 95% CI = 1.37-2.19; dominant genetic model: OR = 1.42, 95% CI = 1.25-1.61; allelic contrast: OR = 1.31, 95% CI = 1.22-1.39, respectively). After restricting our analysis to Chinese individuals, we found that the association was stronger. We also observed strong association between the APO A5 S19>W polymorphism and risk of CAD under a recessive genetic model. This meta-analysis reveals that the minor allele of the -1131T>C polymorphism in the promoter of APO A5 gene significantly increases the susceptibility to CAD. This effect is more pronounced in Chinese subjects.

An experimental and theoretical analysis of molecular separations by diffusion through ultrathin nanoporous membranes.

Diffusion based separations are essential for laboratory and clinical dialysis processes. New molecularly thin nanoporous membranes may improve the rate and quality of separations achievable by these processes. In this work we have performed protein and small molecule separations with 15 nm thick porous nanocrystalline silicon (pnc-Si) membranes and compared the results to 1- and 3- dimensional models of diffusion through ultrathin membranes. The models predict the amount of resistance contributed by the membrane by using pore characteristics obtained by direct inspection of pnc-Si membranes in transmission electron micrographs. The theoretical results indicate that molecularly thin membranes are expected to enable higher resolution separations at times before equilibrium compared to thicker membranes with the same pore diameters and porosities. We also explored the impact of experimental parameters such as porosity, pore distribution, diffusion time, and chamber size on the sieving characteristics. Experimental results are found to be in good agreement with the theory, and ultrathin membranes are shown to impart little overall resistance to the diffusion of molecules smaller than the physical pore size cutoff. The largest molecules tested experience more hindrance than expected from simulations indicating that factors not incorporated in the models, such as molecule shape, electrostatic repulsion, and adsorption to pore walls, are likely important.

Porous nanocrystalline silicon membranes as highly permeable and molecularly thin substrates for cell culture.

Porous nanocrystalline silicon (pnc-Si) is new type of silicon nanomaterial with potential uses in lab-on-a-chip devices, cell culture, and tissue engineering. The pnc-Si material is a 15 nm thick, freestanding, nanoporous membrane made with scalable silicon manufacturing. Because pnc-Si membranes are approximately 1000 times thinner than any polymeric membrane, their permeability to small solutes is orders-of-magnitude greater than conventional membranes. As cell culture substrates, pnc-Si membranes can overcome the shortcomings of membranes used in commercial transwell devices and enable new devices for the control of cellular microenvironments. The current study investigates the feasibility of pnc-Si as a cell culture substrate by measuring cell adhesion, morphology, growth and viability on pnc-Si compared to conventional culture substrates. Results for immortalized fibroblasts and primary vascular endothelial cells are highly similar on pnc-Si, polystyrene and glass. Significantly, pnc-Si dissolves in cell culture media over several days without cytotoxic effects and stability is tunable by modifying the density of a superficial oxide. The results establish pnc-Si as a viable substrate for cell culture and a degradable biomaterial. Pnc-Si membranes should find use in the study of molecular transport through cell monolayers, in studies of cell-cell communication, and as biodegradable scaffolds for three-dimensional tissue constructs.

Methods for controlling the pore properties of ultra-thin nanocrystalline silicon membranes.

Porous nanocrystalline silicon (pnc-Si) membranes are a new class of solid-state ultra-thin membranes with promising applications ranging from biological separations to use as a platform for electron imaging and spectroscopy. Because the thickness of the membrane is only 15-30 nm, on the order of that of the molecules to be separated, mass transport through the membrane is greatly enhanced. For applications involving molecular separations, it is crucial that the membrane is highly permeable to some species while being nearly impermeable to others. An important approach to adjusting the permeability of a membrane is by changing the size and density of the pores. With pnc-Si, a rapid thermal treatment is used to induce nanopore formation in a thin film of nanocrystalline silicon, which is then released over a silicon scaffold using an anisotropic etchant. In this study, we examine the influence of thin film deposition and thermal treatment parameters on pore size and density.

Apolipoprotein C-III can specifically bind to hepatic plasma membranes.

Apo C-III plays an important role in the metabolism of plasma triglyceride, which can delay the catabolism of triglyceride-rich lipoproteins by interfering with apo E-mediated receptor clearance of remnant particles from plasma. The mechanism of the interference has not yet been defined. To further explore the role of apo C-III, we first injected mice with 125I-apo C-III. The measurement of radioactivity showed that liver took up 3.3-10 fold as much radioactivity as other organs such as heart, spleen, lung, kidney, stomach, large intestine, small intestine, and muscle. This was confirmed by incubating the tissue homogenates of the organs with 125I-apo C-III that the radiolabeled apo C-III specifically bound to only hepatic homogenate. To investigate which subcellular part or parts of hepatic cells play the role of binding to apo C-III, hepatic cell components of nucleus, mitochondria, microsomes and plasma membranes were then incubated with 125I-apo C-III. The radiolabeled apo C-III could specifically bind to only hepatic plasma membranes. Finally hepatic plasma membranes were purified to study the characteristics of the specific binding with apo C-III. Addition of increasing concentration of 125I-apo C-III to human hepatic plasma membranes revealed saturable binding to membranes with a Kd of 0.31 +/- 0.07 micromol/l. The maximum specific binding capacity was 1.74 +/- 0.45 microg apo C-III/mg membrane protein. In competition studies using unlabeled apo C-III and isolated lipoproteins HDL, LDL and VLDL, only apo C-III and VLDL effectively competed with 125I-apo C-III for membrane binding. The binding of 125I-apo C-III to human liver plasma membranes was Ca2+-independent, and was abolished when plasma membranes were treated with trypsin. The characteristics of 125I-apo C-III binding to mouse liver plasma membranes were similar to those of human liver plasma membranes with the exception of a binding maximum of 1.52 +/- 0.39 microg apo C-III/mg membrane protein. We conclude that apo C-III exhibits high-affinity binding to hepatic plasma membranes, which is saturable, reverse and specific.

Effect of lipoprotein-X on lipid metabolism in rat kidney.

Lipoprotein-X (Lp-X) is found in the plasma of patients with familial lecithin: cholesterol acyltransferase (LCAT) deficiency syndromes. The majority of the patients with this disorder develop progressive glomerulosclerosis. In this study, the effect of Lp-X on lipid metabolism in perfused rat kidney was investigated. Lp-X was isolated from plasma of patients with familial LCAT deficiency by sequential ultracentrifugation and gel filtration column chromatography. Rat kidneys were perfused for 1-2 h with Krebs-Henseleit buffer containing 20 microM [1-(14)C]acetate or 20 microM [Me-3H]choline. In the presence of Lp-X, no significant difference in the incorporation of radioactivity into triglycerides, cholesterol, phosphocholine, CDP-choline and sphingomyelin was observed. However, incorporation of radioactivity into cholesteryl esters and phosphatidylcholine was significantly elevated in Lp-X perfused kidneys. The contents of cholesterol, cholesteryl esters and phosphatidylcholine were also significantly increased in Lp-X perfused kidneys. The increase in lipid content in the Lp-X perfused kidney is attributed to the direct deposition of Lp-X lipids into the organ. The increase in the labelling of cholesteryl esters was attributed to the increase of available substrate (cholesterol) for the acyl-CoA:cholesterol acyltransferase (ACAT) reaction. The increase in phosphatidylcholine labelling was caused by a reduced turnover of the newly synthesized labelled phosphatidylcholine during Lp-X perfusion.