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Effects of miR-34a expression on cell metastasis-associated protein expression in hepatocellular cells. **P<0.01 vs. control cells. miR, microRNA; miRSCR, scramble miR-34a; SIRT, sirtuin; p53, tumor protein 53, Ac-p53, acetylated p53. [Extracted from the article]

Colorectal cancer (CRC) is a common cancer and the function of long noncoding RNA (lncRNA) AB073614 in CRC mainly unclear. Here, the expression of lncRNA AB073614 in CRC tissues was evaluated by quantitative real-time PCR (qRT-PCR). CCK-8 assays were conducted to explore the impact of AB073614 on cell proliferation. The effects of AB073614 on cell migration, invasion and apoptosis were evaluated by a Transwell in vitro assay. Apoptosis-related molecular marker expression levels were detected by Western blot analysis. In the present study, we confirmed that AB073614 was significantly upregulated in CRC tissues. A difference analysis in the lncRNA AB073614 expression in CRC patient group suggested that the expression of lncRNA AB073614 was independently associated with higher possibilities of high grade ( P = 0.0005), tumor size (> 5 cm) ( P = 0.0001), distant metastasis ( P = 0.0009), and differentiation level ( P = 0.0037). In vitro studies demonstrated that the knockdown of {"type": "entrez-nucleotide", "attrs":{"text": "AB073614", "term&#95;id": "51555790", "term&#95;text": "AB073614"}}AB073614 suppressed SW480 cell proliferation. Meanwhile, the overexpression of {"type": "entrez-nucleotide", "attrs":{"text": "AB073614", "term&#95;id": "51555790", "term&#95;text": "AB073614"}}AB073614 in SW480 cells accelerated cell growth and invasion, and suppressed cell apoptosis. In conclusion, our results suggest that AB073614 may function as a tumor promoter in CRC. Our findings may provide a therapeutic approach for the future treatment of CRC., Competing Interests: None., (IJCEP Copyright © 2019.)

Resolvins, an endogenous lipid mediator derived from eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) of fish oil, has been reported to have anti-inflammatory and antitumor effect in various pathogenic processes. However, there are no studies about the effects of resolvin D1 and E1 on concanavalin A-induced hepatitis. Hence, the present study is to illustrate whether resolvin D1 and E1 inhibit concanavalin A-induced liver injury, liver cancer and underlying mechanisms by which they may recover. C57BL/6 mice were pretreated with resolvin D1 and E1 for 4 h, and then injected with concanavalin A for 12 h. Subsequently, blood and liver tissue were collected at 0, 2, 4, 8 and 12 h for different analysis. Analysis of inflammatory cytokines indicated that the inhibition of necrosis factor (TNF)-α, interferon (IFN)-γ, interleukin (IL)-2, IL-1β and IL-6 could be performed by resolvin D1 and E1. Moreover, Toll-like receptor (TLR) 4 expression, NF-κB and AP-1 activity also have been confirmed to have key roles in the development of liver injury. They were significantly suppressed in the treatment group, compared to model. In addition, resolvin D1 and E1 markedly downregulated CD4+ and CD8+ cell infiltration in the liver. A long-term concanavalin A treatment for 32 weeks was performed to analyze the changes of hepatitis to liver cancer and the antitumor effect of resolving D1 and E1. These results indicated that resolvin D1 and E1 prevent concanavalin A-induced liver injury and the changes of hepatitis to liver cancer in mice through inhibition of inflammatory cytokine secretion and NF-κB/AP-1 activity. Thus, they could be novel target to be considered in the process of finding sufficient drug to protect against various forms of hepatitis and liver cancer.