LINC00606 promotes glioblastoma progression through sponge miR-486-3p and interaction with ATP11B.

BACKGROUND: LncRNAs regulate tumorigenesis and development in a variety of cancers. We substantiate for the first time that LINC00606 is considerably expressed in glioblastoma (GBM) patient specimens and is linked with adverse prognosis. This suggests that LINC00606 may have the potential to regulate glioma genesis and progression, and that the biological functions and molecular mechanisms of LINC00606 in GBM remain largely unknown. METHODS: The expression of LINC00606 and ATP11B in glioma and normal brain tissues was evaluated by qPCR, and the biological functions of the LINC00606/miR-486-3p/TCF12/ATP11B axis in GBM were verified through a series of in vitro and in vivo experiments. The molecular mechanism of LINC00606 was elucidated by immunoblotting, FISH, RNA pulldown, CHIP-qPCR, and a dual-luciferase reporter assay. RESULTS: We demonstrated that LINC00606 promotes glioma cell proliferation, clonal expansion and migration, while reducing apoptosis levels. Mechanistically, on the one hand, LINC00606 can sponge miR-486-3p; the target gene TCF12 of miR-486-3p affects the transcriptional initiation of LINC00606, PTEN and KLLN. On the other hand, it can also regulate the PI3K/AKT signaling pathway to mediate glioma cell proliferation, migration and apoptosis by binding to ATP11B protein. CONCLUSIONS: Overall, the LINC00606/miR-486-3p/TCF12/ATP11B axis is involved in the regulation of GBM progression and plays a role in tumor regulation at transcriptional and post-transcriptional levels primarily through LINC00606 sponging miR-486-3p and targeted binding to ATP11B. Therefore, our research on the regulatory network LINC00606 could be a novel therapeutic strategy for the treatment of GBM.

Identification of key genes in hepatocellular carcinoma associated with exposure to TCDD and α-endosulfan by WGCNA.

2,3,7,8-tet-rachlorodibenzo-p-dioxin (TCDD) and α-endosulfan are two typical persistent organic pollutants (POPs), both of which accumulate in the liver and have potential carcinogenic hepatic effects. The underlying molecular mechanisms of pathogenesis of hepatocellular carcinoma (HCC) remain elusive when exposure to POPs. The aim of this study is to explore the key genes involved in HCC when exposure to TCDD and α-endosulfan by weighted gene co-expression network analysis (WGCNA). First, we performed co-expressed analysis on HCC and normal condition, based on WGCNA. In results, seven co-expressed modules were identified from 56 human liver samples, and the brown module correlated with five stages of HCC. Subsequently, we predicted that human five liver diseases were associated with exposure to TCDD and/or α-endosulfan by Nextbio analysis. Functional enrichment analysis showed that the brown module enriched in oxidation-reduction process, DNA replication, oxidoreductase activity and aging, which were the same as the results when exposure to the mixture of TCDD and α-endosulfan. Lastly, based on the protein-protein interaction network, we identified three novel genes including HK2, EXO1 and PFKP as key genes in HCC associated with exposure to TCDD and α-endosulfan mixture. In addition, survival analysis of key genes in Kaplan-Meier plotter demonstrated that aberrant expression levels of all the three key genes were associated with poor prognosis of HCC. Finally, Western blot analysis confirmed that protein expression levels of PFKP and HK2 in the three exposed groups were significantly elevated, while EXO1 were significantly upregulated when exposure to TCDD and α-endosulfan mixture in HepaRG cells. This study provides a new perspective to the understanding of the genetic mechanism of HCC when exposure to POPs.

The effects of endosulfan on cell migration and invasion in prostate cancer cells via the KCNQ1OT1/miR-137-3p/PTP4A3 axis.

Endosulfan belongs to persistent organic pollutants (POPs), closely related to an increased risk of prostate cancer (PCa). The existing evidence shows that lncRNAs compete with miRNAs for binding sites and contribute to the onset and progression of human malignancies. In this study we investigate how endosulfan promotes cell migration and invasion in DU145 and PC3 prostate cancer cells through epigenetic mechanism of lncRNA-miRNA regulation. Based on our past research we focused on PTP4A3 and constructed wild-type (WT) and mutant PTP4A3 plasmids for further analysis. Our results revealed that transfection of PTP4A3-WT can lead to changes in the expression of epithelial-mesenchymal transition (EMT) biomarkers and critical proteins in the TGF-ß signaling pathway, and promote cell migration and invasion in PCa cells. Bioinformatics analysis shows that there were complementary sequences in PTP4A3 3'-UTR and KCNQ1OT1 3'-UTR to the seed sequence of hsa-miR-137-3p, and dual luciferase reporter assay indicates the potential binding capacity of miR-137-3p to 3'-UTR of PTP4A3 and KCNQ1OT1. We found that miR-137-3p mimic inhibited cell migration and invasion, as well as repressed alterations of EMT biomarkers and critical proteins in the TGF-ß signaling pathway. Rescue experiment results revealed that co-transfection of miR-137-3p mimic and PTP4A3-WT plasmid reversed these changes following transfection with miR-137-3p mimic alone. We found that KCNQ1OT1 was predominantly distributed in the cytoplasm from a subcellular fractionation assay. Functionally, silencing of KCNQ1OT1 repressed cell migration and invasion, and caused alterations of EMT biomarkers and critical proteins in the TGF-ß signaling pathway, which were all restored by co-transfection with anti-miR-137-3p or PTP4A3-WT plasmid. Furthermore, overexpression of miR-137-3p or silencing of KCNQ1OT1 dramatically rescued the effects of endosulfan on promoting cell migration and invasion. These findings suggest that endosulfan can indeed promote cell migration and invasion via the KCNQ1OT1/miR-137-3p/PTP4A3 axis in PCa cells.

Microvirga calopogonii sp. nov., a novel alphaproteobacterium isolated from a root nodule of Calopogonium mucunoides in Southwest China.

In this study, a Gram-negative, rod-shaped, and non-spore-forming bacterium, which was designated as strain CCBUA 65841T, was isolated from a root nodule of Calopogonium mucunoides grown in Yunan Province of China. The sequence alignment results of 16S rRNA and four housekeeping genes (including gyrB, recA, dnaK and rpoB) indicated the isolated strain is a member of the genus Microvirga, closely related to Microvirga lotononidis WSM3557T. In addition, results of genome average nucleotide identity (ANI) and digital DNA-DNA hybridization (dDDH) had revealed the lower values (ANI ≤ 88.72%, dDDH ≤ 39.5%) between strain CCABU 65841T and other related Microvirga species. The genome of the novel strain exhibits a G + C content of 64.48% and contains 7296 protein-coding genes and 93 RNA genes. The major polar lipids were found to be phosphatidylcholine and phosphatidylethanolamine. The predominant cellar fatty acids were identified to be C16:0, C18:0, C19:0 cyclo ω8c, summed feature 2, summed feature 3 and summed feature 8. Moreover, menaquinone 8 (MK-8) was detected to be the predominant quinone. Based on the phylogenetic and phenotypic dissimilarity, a novel species Microvirga calopogonii sp. nov. is proposed with the type strain CCABU 65841T (= LMG 25488 T = HAMBI 3033T).

Effects of graft copolymer of chitosan and salicylic acid on reducing rot of postharvest fruit and retarding cell wall degradation in grapefruit during storage.

This study was to evaluate the effect of graft copolymer (CTS-g-SA) of chitosan (CTS) and salicylic acid (SA) on the storability of grapefruit fruits during postharvest storage. Results indicate that the graft copolymer treatment significantly depressed green mold caused by Penicillium digitatum. The graft copolymer application kept fruit firmness without impairing the fruit quality. Moreover, the graft copolymer treatment inhibited the activity and gene expression of cell wall-modifying enzymes such as polygalacturonase, cellulase, pectin methylesterase, α-l-arabinofuranosidase, ß-galactosidase, and suppressed the modification of cell wall components including covalently bound polysaccharide (sodium carbonate soluble pectin, 24% KOH-soluble fraction), which were associated with fruit softening. These results suggested that graft copolymer application can be recognized as a postharvest technique to suppress rotting and delay softening through inhibiting solubilization of cell wall polysaccharides.

Recovery of Populus tremuloides seedlings following severe drought causing total leaf mortality and extreme stem embolism.

In contrast with other native Populus species in North America, Populus tremuloides (aspen) can successfully establish itself in drought-prone areas, yet no comprehensive analysis has been performed on the ability of seedlings to withstand and recover from a severe drought resulting in complete leaf mortality. Here, we subjected 4-month-old aspen seedlings grown in two contrasting soil media to a progressive drought until total leaf mortality, followed by a rewatering cycle. Stomatal conductance (g(s) ), photosynthesis and transpiration followed a sigmoid decline with declining fraction of extractable soil water values. Cessation of leaf expansion occurred close to the end of the linear-decrease phase, when g(s) was reduced by 95%. Leaf mortality started after g(s) reached the lowest values, which corresponded to a stem-xylem pressure potential (Ψ(xp)) of -2.0 MPa and a percent loss of stem hydraulic conductivity (PLC) of 50%. In plants with 50% leaf mortality, PLC values remained around 50%. Complete leaf mortality occurred at an average stem PLC of 90%, but all seedlings were able to resprout after 6-10 days of being rewatered. Plants decapitated at soil level before rewatering developed root suckers, while those left with a 4-cm stump or with their stems intact resprouted exclusively from axillary buds. Resprouting was accompanied by recovery of stem hydraulic conductivity, with PLC values around 30%. The percentage of resprouted buds was negatively correlated with the stem %PLC. Thus, the recovery of stem hydraulic conductivity appears as an important factor in the resprouting capacity of aspen seedlings following a severe drought.