Lung cancer is a lethal cancer that threatens human health. Several studies have demonstrated the role of long non-coding RNAs (lncRNAs) in lung cancer. SOX21-AS1 is a newly discovered oncogenic lncRNA, but its molecular mechanism in lung cancer is not known. Here, the levels of SOX21-AS1, miR-24-3p, and PIM2 were examined in lung cancer and normal tissues. The relationships between miR-24-3p and SOX21-AS1 or PIM2 were predicted using bioinformatics tools and confirmed using a luciferase reporter assays. Colony formation, MTT, flow cytometry, and transwell assays were conducted to analyze cell proliferation, apoptosis, migration, and invasion abilities, respectively. Western blotting was used to measure PIM2 expression levels in cancer tissues and cells. SOX21-AS1 expression levels were high in lung cancer tissues and cells. In contrast, the amount of miR-24-3p bound to SOX21-AS1 was relatively low in cancerous tissues and cells. The knockdown of SOX21-AS1 decreased cell proliferation, activated apoptosis, and promoted cell migration and invasion. These effects were abolished by miR-24-3p inhibition. The oncogenic function of SOX21-AS1 mediated through targeting miR-24-3p was also demonstrated in animal models. PIM2 was targeted by miR-24-3p and showed increased levels in tumor tissues and cells. Furthermore, miR-24-3p overexpression inhibited the proliferation and promoted the apoptosis of lung cancer cells. In lung cancer cells, SOX21-AS1 negatively modulated the miR-24-3p/PIM2 axis to facilitate their proliferation, migration, and invasion. These findings offer a novel idea for future research on treating lung cancer at the molecular level.

Mesenchymal stem cells (MSCs) were shown to have potential therapeutic effects for treatment of liver fibrosis, and dysregulated expression of microRNAs (miRNAs) played a pivotal role in the pathogenesis of liver fibrosis by regulating their downstream target genes. However, the mechanism by which MSCs affect the progression of liver fibrosis by regulating miRNA expression remains unclear. Here, we investigated whether human umbilical cord MSCs (HUC-MSCs) attenuated hepatic fibrosis by regulating miR-455-3p and its target gene. Significantly upregulated miRNA (miR-455-3p) was screened out by GEO datasets analysis and coculture HUC-MSCs with hepatic stellate cell (HSC) LX-2 cells. p21-activated kinase-2 (PAK2) was forecasted to be the target gene of miR-455-3p by bioinformatics analyses and confirmed by luciferase reporter assay. HUC-MSCs were transplanted into mice with carbon tetrachloride- (CCl4-) induced liver fibrosis, the result showed that HUC-MSC transplantation significantly ameliorated the severity of CCl4-induced liver fibrosis, attenuated collagen deposition, improved liver function by reducing the expression of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum, upregulated miR-455-3p, and suppressed PAK2 expression of liver tissue in mice. Taken together, our study suggests that HUC-MSCs inhibit the activation of HSCs and mouse CCl4-induced liver fibrosis by upregulation of miR-455-3p through targeting PAK2.

Background Mesenchymal stem cells (MSCs) are considered to be a potential therapeutic tool for liver fibrosis. Inhibiting the activation of hepatic stellate cells (HSCs) and protecting hepatocytes are important mechanisms for the anti-fibrotic effect of MSCs. However, how MSCs inhibit liver fibrosis by regulating the expression of microRNAs (miRNAs) has not been fully clarified. Methods Transforming growth factor-β1 (TGF-β1)-activated HSCs LX-2 were single cultured or co-cultured with human umbilical cord mesenchymal stem cells (HUC-MSCs). High-throughput sequencing was used to evaluate the differentially expressed microRNAs (DEMs) between the two groups. Quantitative real-time PCR (qRT-PCR), Western blot, and transfection experiments were used to investigate and screen the most significantly up-regulated DEM. Bioinformatics analysis was used to predict the target mRNAs and the potential functions of the DEM. The possible mechanism of HUC-MSCs against liver fibrosis was analyzed by co-culture experiment of HUC-MSCs with LX-2 cells, and HUC-MSCs treatment of Bile duct ligation (BDL)-induced liver fibrosis in mice. Finally, the mechanism of the DEM regulating liver fibrosis was confirmed in human liver fibrosis specimens. Results MicroRNA-148a-5p (miR-148a-5p) was the most significantly up-regulated DEM in activated LX-2 cells co-cultured with HUC-MSCs compared with LX-2 cells single cultured. Up-regulation of the expression of miR-148a-5p in activated LX-2 cells could significantly inhibit the expression of hepatic fibrosis markers α-SMA and Col1α1. Notch2 was one target gene of miR-148a-5p. Co-cultured with HUC-MSCs could inhibit the activation of LX-2 cells by inhibiting the expression of the Notch2 and the Notch signaling pathway. In addition, HUC-MSCs treatment could up-regulate the expression of miR-148a-5p in liver tissue and hepatocytes, promote the proliferation and avoid the apoptosis of hepatocytes, and reduce the degree of fibrosis by inhibiting expression of the Notch2 and the Notch signaling pathway in BDL-induced liver fibrosis mice. Moreover, miR-148a-5p was down-regulated and Notch2 was up-regulated in fibrotic human liver tissues compared with the normal livers. Conclusions HUC-MSCs treatment could inhibit HSCs activation, protect hepatocytes, and alleviate BDL-induced liver fibrosis in mice by up-regulating the expression of miR-148-5p and inhibiting the Notch signaling pathway. The down-regulation of miR-148-5p and up-regulation of Notch2 could be used as biomarkers to monitor the progression of liver fibrosis.

Equilibrium isotherms of Cr(VI) uptake by tobacco-leaf residues, under controlled solution pH and temperature, were obtained with batch uptake experiments. Batch uptake kinetics under different initial Cr(VI) concentrations was also obtained. The results showed that Cr(VI) uptake capacities of the tobacco-leaf residues were up to 113.2 mg g(-1) (dry wt). The uptake capacity was found to be dependent on solution pH and the maximum values were obtained at a pH of around 1.0. On the other hand, the effect of temperature the uptake capacity was found to be small. All equilibrium isotherms were well correlated with the standard Langmuir equation. Kinetics profiles showed that the uptake process was fast, and equilibrium was reached within 30 minutes of mixing contact. The role of polyphenols in Cr(VI) biosorption was studied and the results indicated that complex formation with Cr(VI) may be an important mechanism for Cr(VI) removal. The study indicated that abundantly available tobacco-leaf residues can be used as efficient biosorbent materials for Cr(VI) removal from wastewater.

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