Degradation characteristics of polybutylene adipate terephthalic acid (PBAT) and its effect on soil physicochemical properties: A comparative study with several polyethylene (PE) mulch films.

The degradation process of different types of mulch in agriculture and its effect on soil ecosystem should be considered comprehensively. To this end, the changes in performance, structure, morphology, and composition of PBAT film during the degradation process were examined through a multiscale approach in comparison with several PE films and their effects on the soil physicochemical properties were investigated. At the macroscopic scale, the load and elongation of all films decreased with increasing ages and depths. At the microscopic scale, the stretching vibration peak intensity (SVPI) for PBAT and PE films decreased by 48.8 âˆ¼ 60.2% and 9.3 âˆ¼ 38.6%, respectively. The crystallinity index (CI) increased by 67.3 âˆ¼ 209.6% and 15.6 âˆ¼ 21.8%, respectively. At the molecules scale, terephthalic acid (TPA) was detected in localized soil with PBAT mulch after 180 d. In short, the degradation characteristics of PE films were depended on their thickness and density. The PBAT film exhibited the highest degree of degradation. Simultaneously, the soil physicochemical properties such as soil aggregates, microbial biomass and pH were affected by the changes of film structure and components during the degradation process. This work has practical implications for the sustainable development of agriculture.

ATDC contributes to sustaining the growth and invasion of glioma cells through regulating Wnt/ß-catenin signaling.

Accumulating evidence has documented that ataxia-telangiectasia group D complementing gene (ATDC) is aberrantly expressed in various cancers and is associated with cancer development and progression. However, little is known about the role of ATDC in glioma tumorigenesis. In this study, we aimed to explore the biological function and regulatory mechanism of ATDC in glioma. We found that ATDC expression was highly upregulated in glioma cell lines. Knockdown of ATDC significantly inhibited the growth and invasion of glioma cells. In contrast, overexpression of ATDC markedly promoted the growth and invasion of glioma cells. Moreover, our results showed that inhibition of ATDC reduced the expression levels of Dishevelled 2 (Dvl2) and ß-catenin and impeded the activation of Wnt/ß-catenin signaling, whereas overexpression of ATDC showed the opposite effect. Knockdown of Dvl2 significantly blocked the promotion effect of ATDC overexpression on activation of Wnt/ß-catenin signaling. In addition, silencing of ß-catenin partially reversed the oncogenic effect of ATDC overexpression in glioma cells. Taken together, out study reveals an oncogenic role of ATDC that drives the growth and invasion of glioma by modulating the Wnt/Dvl2/ß-catenin signaling pathway, suggesting a potential therapeutic target for treatment of glioma.

CREPT promotes glioma cell proliferation and invasion by activating Wnt/ß-catenin pathway and is a novel target of microRNA-596.

Cell cycle-related and expression elevated protein in tumor (CREPT) is emerging as a novel cancer-related gene that is dysregulated in many kinds of malignancies. However, the expression and biological role of CREPT in glioma remains unclear. In the present study, we aimed to explore the potential function and regulation mechanism of CREPT in glioma. Results showed that CRETP expression was significantly upregulated in glioma cell lines. Depletion of CREPT by siRNA-mediated gene silencing markedly decreased the proliferative and invasive capabilities of glioma cells. Bioinformatics analysis predicted CREPT as a target gene of microRNA-596 (miR-596), which was further verified by real-time quantitative polymerase chain reaction and Western blot analysis. miR-596 was significantly decreased in glioma tissues and cell lines, and inversely correlated with CREPT expression in clinical specimens. Knockdown of CREPT or overexpression of miR-596 significantly restricted the activation of Wnt/ß-catenin signaling in glioma cells. Moreover, overexpression of CREPT partially reversed the miR-596-mediated inhibitory effect on proliferation, invasion and Wnt/ß-catenin signaling in glioma cells. Overall, these results demonstrate that CREPT exerts an oncogenic role in glioma and its expression is regulated by miR-596. Our study highlights the important role miR-596/CREPT/Wnt/ß-catenin signaling axis may play in glioma.

MicroRNA-520e restricts the proliferation and invasion of glioma cells through the downregulation of Wnt/ß-catenin signaling by targeting fibroblast growth factor 19.

The abnormal expression of microRNAs (miRNAs) contributes to the development and progression of cancer. Recent studies have reported that miRNA-520e (miR-520e) is dysregulated in multiple cancers and is associated with tumor progression. However, the role of miR-520e in glioma has not been fully investigated. In this study, we investigated the function of miR-520e and its regulation by a molecular mechanism in gliomas. Our results showed that miR-520e expression was significantly downregulated in glioma tissues and cell lines. The overexpression of miR-520e repressed the proliferation, colony formation, and invasive potential of glioma cells, while the inhibition of miR-520e showed the opposite effect. The oncogenic gene fibroblast growth factor 19 (FGF19) was identified as a downstream target gene of miR-520e. The knockdown of FGF19 restricted the proliferation and invasion of glioma cells. Moreover, FGF19 knockdown or miR-520e overexpression decreased the expression of ß-catenin and suppressed the transcriptional activity of Wnt/ß-catenin signaling. Notably, the restoration of FGF19 expression partially reversed the miR-520e-mediated antitumor effect. In conclusion, our results demonstrate that miR-520e restricts the proliferation and invasion of glioma cells through the downregulation of FGF19/Wnt/ß-catenin signaling, highlighting an importance of miR-520e/FGF19/Wnt/ß-catenin signaling in gliomagenesis and suggesting miR-520e as a potential therapeutic target for gliomas.

Long noncoding RNA-RNCR3 overexpression deleteriously affects the growth of glioblastoma cells through miR-185-5p/Krüppel-like factor 16 axis.

Glioblastoma (GBM) is a devastating and highly aggressive tumor, which is apoptosis resistant and difficult to cure. Recently, long noncoding RNAs have been shown to play a pivotal role in GBM progression. Evidence has suggested that retinal noncoding RNA3 (RNCR3) is a GBM-associated noncoding RNA and is under-expressed in GBM. However, the function and mechanism of RNCR3 on GBM cell growth and apoptosis are still uncertain. In the current study, we found that the level of RNCR3 is decreased in U87, U251, U373, and A172 GBM cell lines when compared with the normal human astrocytes. Elevating long noncoding RNA RNCR3 expression markedly inhibits U87 and U251 cell survival and proliferation. Further studies indicated that RNCR3 overexpression promotes U87 and U251 cell apoptosis and activity caspase-3/7. Moreover, we found that RNCR3 overexpression promotes Krüppel-like factor 16 (KLF16) expression through inhibiting the level of miR-185-5p. We demonstrated that KLF16 is a direct target of miR-185-5p. An increased miR-185-5p level by a miR-185-5p mimic or decreased KLF16 by KLF16 small interfering RNA both reversed the function of RNCR3 overexpression on GBM cell growth and apoptosis. In summary, this study focuses on investigating the key molecular mechanisms of RNCR3 involved in GBM cell growth and apoptosis. Our data indicated that RNCR3 overexpression inhibits cell growth and induces its apoptosis through the miR-185-5p/KLF16 axis.

MicroRNA-409-3p Represses Glioma Cell Invasion and Proliferation by Targeting High-Mobility Group Nucleosome-Binding Domain 5.

Emerging evidence has suggested that aberrantly expressed microRNAs (miRNAs) are associated with glioma development and progression. The aberrant expression of miR-409-3p has been reported in several human cancers. However, little is known about the function of miR-409-3p in gliomas. The aim of this study was to investigate the specific role and molecular mechanism of miR-409-3p in gliomas. In the present study, we found that miR-409-3p was downregulated in glioma tissue and cell lines. Overexpression of miR-409-3p inhibited glioma cell invasion and proliferation, whereas suppression of miR-409-3p promoted glioma cell invasion and proliferation. High-mobility group nucleosome-binding domain 5 (HMGN5), a well-known oncogene in gliomas, was identified as a functional target of miR-409-3p using bioinformatics, dual-luciferase reporter assay, real-time quantitative polymerase chain reaction, and Western blot analysis. Furthermore, miR-409-3p was found to regulate the expression of matrix metalloproteinase 2 and cyclin D1. Restoration of HMGN5 expression significantly reversed the inhibitory effects of miR-409-3p overexpression on glioma cell invasion and proliferation. Taken together, our results suggest that miR-409-3p inhibits glioma cell invasion and proliferation by targeting HMGN5, representing a potential therapeutic target for glioma.

Neuroprotective effects of syringic acid against OGD/R-induced injury in cultured hippocampal neuronal cells.

Cerebral ischemic injury and treatment are important topics in neurological science. In the present study, an in vitro model of cerebral ischemia was established by subjecting primary cultures of hippocampal neuronal cells to oxygen-glucose deprivation followed by reperfusion (OGD/R), in order to evaluate the possible neuroprotective role of syringic acid (SA). The results of 3-(4,5-dimethylthiazol­2-yl)-2,5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays showed that pre-treatment with SA (0.1, 1, 10, and 20 µM) attenuated OGD/R-induced neuronal injury in a dose-dependent manner, with evidence of increased cell viability and decreased LDH leakage. In addition, oxidative stress markers were evaluated using commercial kits, and the results demonstrated that OGD/R exposure induced distinct oxidative stress, accompanied by elevated levels of intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) production, and reduced activity of the antioxidant enzyme superoxide dismutase (SOD), which were dose-dependently restored by pre-treatment with SA. In addition, the concentration of intracellular free calcium [Ca2+]i and mitochondrial membrane potential (MMP or Δψm) were determined in order to evaluate the degree of neuronal damage by performing flow cytometric analysis and observing the cells under a fluorescence microscope, respectively. We demonstrated that pre-treatment with SA inhibited elevations in [Ca2+]i, whereas it increased the MMP dose-dependently following exposure to OGD/R. Western blot analysis revealed that OGD/R promoted cell apoptosis with concomitant increases in Bax and caspase-3 expression, and reduced Bcl-2 expression, which was reversed by pre­treatment with SA in a dose-dependent manner. Moreover, these effects were mediated through the JNK and p38 pathways, as pre­treatment with SA inhibited the OGD/R-induced increase in phosphorylated (p-)JNK and p-p38 expression. Taken together, these results suggested that SA exerted strong neuroprotective effects in hippocampal neuronal cells, which may be attributed to the attenuation of OGD/R-induced cell injury through the JNK and p38 signaling pathways.