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Objective To investigate the effects of eukaryotic elongation factor-2 kinase (eEF2K) gene transfection and sodium tanshinone Ⅱ A sulfonate (STS) on proliferation, invasion and migration of lung adenocarcinoma cell line A549 and its mechanism. Methods The optimal concentration of STS was screened out by preliminary experiment. A549 cells were divided into siRNA-NC group (transfected with siRNA-NC), siRNA-eEF2K group (transfected with siRNA-eEF2K), siRNA-NC+STS group (treated with 10 μg/mL STS after siRNA-NC) and siRNA-eEF2K+STS group (treated with 10 μg/mL STS after siRNA-eEF2K).The survival rate, clone formation, cell counting of transmembrane cells, migration and apoptosis of A549 cells were detected by CCK-8 method, clone formation test, Transwell chamber test, scratch test and flow cytometry. The protein expression levels of protein kinase B (AKT), phosphorylation (p)-AKT, Ki67, matrix metalloproteinase-2 (MMP-2) and B-cell lymphoma-2 genes (Bcl-2) were detected by Western blot. Results Compared with those in siRNA-NC group, the cell survival rate, clone formation rate, number of transmembrane cells, migration rate and p-AKT, Ki67, MMP-2 and Bcl-2 in proteins siRNA-eEF2K+STS group were significantly lower, while the apoptosis rate was significantly higher (P＜0.05). The siRNA-eEF2K+STS group had the largest range of changes in the above indexes. Conclusions Silencing eEF2K combined with STS can synergistically inhibit the proliferation, invasion and migration of A549 cells and promote cell apoptosis. The mechanism is potentially related to the inhibition of protein expression of p-AKT, Ki67, MMP-2 and Bcl-2.

Objective To investigate the effect of triptolide (TP) on the proliferation and apoptosis of human non-small cell lung cancer cell A549 by regulating the expression of chemokine receptor 4 (CXCR4) gene. Methods The experiment was divided into 4 groups: control group, TP group (100 nm/L TP-treated cells), CXCR4+TP group (transfected plasmid TP-treated cells) and NC+TP group (empty plasmid TP-treated cells). The expression of CXCR4 and transfection were detected by RT-qPCR and Western blot. Cell proliferation was detected by MTT assay, apoptosis was detected by Annexin V-FITC/PI double staining, proliferation and apoptosis-related protein expression were detected by Western blot. Results Triptolide inhibited the expression of CXCR4 mRNA and protein in A549 cells (P＜0.05). Triptolide inhibited the proliferation of A549 cells and induced apoptosis(P＜0.05). Transfection of pcDNA-CXCR4 up-regulated the expression of CXCR4 mRNA and protein (P＜0.05). Up-regulation of CXCR4 expression partially reversed the effect of triptolide on proliferation inhibition and apoptosis induction of A549 cells (P＜0.05). Conclusions Triptolide may inhibit the proliferation of non-small cell lung cancer A549 cells and induce apoptosis by down-regulating the expression of CXCR4.

Structure and acidity changes of the acid sites in ultra-stable Y zeolites of different cell sizes during the hydrothermal aging process were studied by solid-state nuclear magnetic resonance (NMR) combined with molecular probes. The experimental results demonstrated that, during the initial stage of hydrothermal aging, parts of the framework aluminum species were removed from the framework and formed five-coordinate extra-framework aluminum species. In the meanwhile, the five-coordinate extra-framework aluminum species migrated to the surface and formed poly-aluminum species, resulting in decreases of both Brønsted acid sites and Lewis acid sites. The acidity of ultra-stable Y zeolites changed considerably during the first 3 h of the aging process, and the change of Brønsted acid content was proportional to the unit cell dimension of the fresh zeolites agent. With the increase of aging time, the aluminum distribution tended to become stable, with little further changes in the amounts of Brønsted acid and Lewis acid sites. The synergy between Brønsted/Lewis acids in the ultra-stable Y zeolites existed during the entire aging process, resulting in a stably enhanced acidity for the Brønsted acid sites.

In order to investigate the relationship between 137Cs and soil total carbon (TC) in artificial forests, a study was conducted on Platycladus orientalis forest (PO), Quercus variabilis forest (QV), and abandoned land slope. Results demonstrated that both PO and QV have higher levels of 137Cs and lower TC stocks compared to the abandoned land slope. There is a significant correlation between 137Cs and TC in artificial forests, suggesting that 137Cs can be used as a reliable tracer for TC migration in afforestation areas. However, it is not recommended to use 137Cs for estimating TC in abandoned land slopes. [ABSTRACT FROM AUTHOR]

Sodium tanshinone IIA sulphate (STS) is a product originated from Salvia miltiorrhiza Bunge [Lamiaceae], which exerts an antitumour effect. However, the role of STS on lung adenocarcinoma (LUAD) remains unexplored. Our study explores the effect and mechanism of STS against LUAD. LUAD cells were treated with 100 μM STS for 24 h and control group cells were cultured under normal medium conditions. Functionally, the viability, migration, invasion and angiogenesis of LUAD cells were examined by MTT, wound healing, transwell and tube formation assay, respectively. Moreover, cells were transvected with different transfection plasmids. Dual luciferase reporter and RNA immunoprecipitation (RIP) assays were used to verify the relationship between miR-874 and eEF-2K. STS significantly decreased the viability (40–50% reduction), migration (migration rate of A549 cells from 0.67 to 0.28, H1299 cells from 0.71 to 0.41), invasion (invasion numbers of A549 cells from 172 to 55, H1299 cells from 188 to 35) and angiogenesis (80-90% reduction) of LUAD cells. Downregulation of miR-874 partially abolished the antitumour effect of STS. EEF-2K was identified to be the target of miR-874, and its downregulation markedly abolished the effects of miR-874 downregulation on tumourigenesis of LUAD. Moreover, silencing of TG2 abrogated eEF-2K-induced progression of LUAD. STS attenuated the tumourigenesis of LUAD through the mediation of the miR-874/eEF-2K/TG2 axis. STS is a promising drug to fight against lung cancer, which might effectively reverse drug resistance when combined with classical anticancer drugs. [ABSTRACT FROM AUTHOR]

Lung cancer (LCa), the most frequent malignancy worldwide, causes millions of mortalities each year. Overexpression of the long noncoding RNA MIR210HG in LCa has been established; however, a more comprehensive investigation into its biological role within LCa is imperative. This study aimed to validate the MIR210H levels in LCa tissues and cells. The expression of indicated genes was evaluated using quantitative real‐time polymerase chain reaction (qRT‐PCR) and/or Western blotting. The viability, proliferation, migration, and invasion of LCa cells were measured using the 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyl tetrazolium bromide (MTT), colony formation, wound healing, and transwell assays, respectively. The methylation levels of LCa cells were determined via methylation‐specific PCR; additionally, chromatin immunoprecipitation or RNA immunoprecipitation assays were performed to determine the targeting relationship between DNA methyltransferase 1 (DNMT1) and the SH3‐domain containing CRB2 like 3 (SH3GL3) promoters and the interaction between DNMT1 and MIR210HG, respectively. Our findings revealed the upregulation of MIR210HG, coupled with a diminished expression of SH3GL3 in LCa tissues and cells. Knockdown of MIR210HG or overexpression of SH3GL3 suppressed the proliferative, migratory, and invasive capacities of the cells. DNMT1 bound to the SH3GL3 promoter region, and MIR210HG inhibited the transcription of SH3GL3 by recruiting DNMT1. These findings indicate that MIR210HG facilitates LCa cell growth and metastasis by repressing SH3GL3 transcription via the recruitment of DNMT1 to the SH3GL3 promoter region. [ABSTRACT FROM AUTHOR]