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There is increasing evidence that circular RNA (circ RNA) are involved in cancer development, but the regulation and function of human circ RNA remain largely unknown. In this study, we demonstrated that ZKSCAN1, a zinc finger family gene, is expressed in both linear and circular ( circ ZKSCAN1) forms of RNA in human hepatocellular carcinoma ( HCC) tissues and cell lines. Here, we analyzed a cohort of 102 patients and found that expression of both ZKSCAN1 mRNA and circ ZKSCAN1 was significantly lower ( P < 0.05) in the HCC samples compared with that in matched adjacent nontumorous tissues by reverse transcription PCR ( RT- PCR). The low expression level of ZKSCAN1 was only associated with tumor size ( P = 0.032), while the cir ZKSCAN1 levels varied in patients with different tumor numbers ( P < 0.01), cirrhosis ( P = 0.031), vascular invasion ( P = 0.002), or microscopic vascular invasion ( P = 0.002), as well as with the tumor grade ( P < 0.001). Silencing both ZKSCAN1 mRNA and circ ZKSCAN1 promoted cell proliferation, migration, and invasion. In contrast, overexpression of both forms of RNA repressed HCC progression in vivo and in vitro. Silencing or overexpression of both forms of RNA did not interfere with each other. RNA-seq revealed a very different molecular basis for the observed effects; ZKSCAN1 mRNA mainly regulated cellular metabolism, while circ ZKSCAN1 mediated several cancer-related signaling pathways, suggesting a nonredundant role for ZKSCAN1 mRNA and circ RNA. In conclusion, our results revealed two post-translational products ( ZKSCAN1 mRNA and circ ZKSCAN1) that cooperated closely with one another to inhibit growth, migration, and invasion of HCC. cir ZKSCAN1 might be a useful marker for the diagnosis of HCC. [ABSTRACT FROM AUTHOR]

There is increasing evidence that circular RNA (circRNA) are involved in cancer development, but the regulation and function of human circRNA remain largely unknown. In this study, we demonstrated that ZKSCAN1, a zinc finger family gene, is expressed in both linear and circular (circZKSCAN1) forms of RNA in human hepatocellular carcinoma (HCC) tissues and cell lines. Here, we analyzed a cohort of 102 patients and found that expression of both ZKSCAN1mRNA and circZKSCAN1 was significantly lower (P < 0.05) in the HCC samples compared with that in matched adjacent nontumorous tissues by reverse transcription PCR (RT-PCR). The low expression level of ZKSCAN1 was only associated with tumor size (P = 0.032), while the cirZKSCAN1 levels varied in patients with different tumor numbers (P < 0.01), cirrhosis (P = 0.031), vascular invasion (P = 0.002), or microscopic vascular invasion (P = 0.002), as well as with the tumor grade (P < 0.001). Silencing both ZKSCAN1mRNA and circZKSCAN1 promoted cell proliferation, migration, and invasion. In contrast, overexpression of both forms of RNA repressed HCC progression in vivo and in vitro. Silencing or overexpression of both forms of RNA did not interfere with each other. RNA-seq revealed a very different molecular basis for the observed effects; ZKSCAN1mRNA mainly regulated cellular metabolism, while circZKSCAN1 mediated several cancer-related signaling pathways, suggesting a nonredundant role for ZKSCAN1mRNA and circRNA. In conclusion, our results revealed two post-translational products (ZKSCAN1mRNA and circZKSCAN1) that cooperated closely with one another to inhibit growth, migration, and invasion of HCC. cirZKSCAN1 might be a useful marker for the diagnosis of HCC., (© 2017 The Authors. Published by FEBS Press and John Wiley & Sons Ltd.)

Purpose: The present study aimed to investigate the potential association between the urokinase plasminogen activation (uPA) system polymorphisms (rs4065, rs2227564, and rs344781) and cancer risk., Methods: An extensive search was performed to identify published case-control studies on the association between the uPA system polymorphisms and cancer risk. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to evaluate the relationship between the uPA system polymorphisms and cancer risk., Results: A total of 20 studies comprising 7,037 cancer cases and 10,094 controls were identified and included in the present meta-analysis. Overall, significantly increased cancer risk was associated with the uPA polymorphism rs4065 (T vs C: OR 1.50, 95% CI: 1.19-1.89; TT vs CC: OR 4.63, 95% CI: 3.10-6.91; dominant model: OR 1.93, 95% CI: 1.60-2.33; recessive model: OR 3.02, 95% CI: 1.26-7.25) and the uPA receptor polymorphism rs344781 (T vs C: OR 1.13, 95% CI: 1.04-1.23; TC vs CC: OR 1.26, 95% CI: 1.06-1.49; TT vs CC: OR 1.35, 95% CI: 1.13-1.63; dominant model: OR 1.29, 95% CI: 1.10-1.52). No significant association was found between the uPA polymorphism rs2227564 and cancer risk. Subgroup analysis suggests that the T allele of the rs4065 (T allele vs C allele: OR 1.50, 95% CI: 1.19-1.89) and rs344781 polymorphisms (T allele vs C allele: OR 1.13, 95% CI: 1.04-1.23) was associated with increased cancer risk in Asians., Conclusion: Our results suggest that the uPA polymorphism rs4065 and the uPA receptor polymorphism rs344781 are associated with increased cancer risk.

To evaluate the effects of alginate scaffold-bone marrow stromal cell (BMSC) in the treatment of acute liver failure in rats and provide a basis for in vivo application of artificial liver tissue. CM-DiI-labeled BMSCs were planted and grown on alginate scaffolds to form alginate scaffold-BMSC complex. Alginate scaffold-BMSC complex (the experimental group) or alginate scaffolds (the control group) were placed onto the surface of liver wound of rats after 70% of hepatectomy. The scaffold-BMSC complex and alginate scaffolds were removed after 4 weeks and fluorescence microscopy was used to track the growth and distribution of CM-DiI-labeled BMSCs. The liver tissues were stained for albumin and glycogen to investigate the differentiation of BMSCs on alginate scaffolds. The survival rate and liver function were also compared between the two groups of rats. BMSCs on alginate scaffolds and liver tissues were clearly demonstrated by CM-DiI labeling. BMSCs on alginate scaffolds secreted albumin and produced glycogen. The survival rate and liver function of the rats of the experimental group were significantly higher than that the control group rats. Alginate scaffold-BMSC complex promotes the regeneration of liver tissues in rats of acute liver failure.

Objectives: This study aims to explore whether Huperzine A (HupA) could protect neural stem cells against amyloid beta-peptide Aβ induced apoptosis in a neural stem cells (NSCs) and microglia co-culture system., Methods: Rat NSCs and microglial cells were isolated, cultured and identified with immunofluorescence Assays (IFA). Co-culture systems of NSCs and microglial cells were employed using Transwell Permeable Supports. The effects of Aβ1-42 on NSCs were studied in 4 groups using co-culture systems: NSCs, Aβ+NSCs, co-culture and Aβ+co-culture groups. Bromodeoxyuridine (BrdU) incorporation and flow cytometry were utilized to assess the differences of proliferation, differentiation and apoptosis of NSCs between the groups. LQ test was performed to assess the amounts of IL-6, TNF-α and MIP-α secreted, and flow cytometry and Western blotting were used to assess apoptosis of NSCs and the expressions of Bcl-2 and Bax in each group., Results: IFA results showed that isolated rat NSCs were nestin-positive and microglial cells were CD11b/c-positive. Among all the groups, the Aβ+co-culture group has the lowest BrdU expression level, the lowest MAP2-positive, ChAT-positive cell counts and the highest NSC apoptosis rate. Smaller amounts of IL-6, TNF-α and MIP-α were being secreted by microglial cells in the HupA+Aβ+co-culture group compared with those in the Aβ+ co-culture group. Also the Bcl-2: Bax ratio was much higher in the HupA+Aβ+co-culture group than in the Aβ+co-culture group., Conclusions: HupA inhibits cell apoptosis through restraining microglia's inflammatory response induced by Aβ1-42.