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SummaryFog computing is a new computing paradigm that can provide flexible resources and services at the edge of network. It is an extension of cloud computing and usually cooperated with cloud computing. Therefore, end users, fog nodes, and cloud servers can form a three‐layer service model in practical application. In this model, they should have an agreement on a service contract, which contains every party's rights and obligations before the beginning of the service. However, due to lack of trust, it will suffer from some fairness problems during signing a service contract. Contract signing protocol allows two or more mutual distrust entities to sign a predefined digital contract in a fair and effective way. In this paper, we propose a fair three‐party contract signing protocol based on the primitive of blockchain, which can be applied to the scenario of fog computing. Our proposed construction allows the participants to sign a contract in a fair way without the involvement of an arbitrator. Moreover, the privacy of the contract content can be preserved on the public chain. Finally, we realize the proposed protocol through the private blockchain and provide the experimental simulation that analyzes the efficiency and effectiveness.

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Hepatocellular carcinoma (HCC) is the fifth most common cancer type worldwide and the third leading cause of cancer-associated mortality. To date, its pathogenesis has remained poorly understood. Previous studies have demonstrated that deregulated microRNA (miR) participates in hepatocarcinogenesis. In the present study, miR-218 and miR-520a were observed to be downregulated in human HCC cells relative to normal hepatic cells. Overexpression of miR-218 or miR-520a inhibited cell proliferation and induced cell cycle arrest at the G0/G1 phase checkpoint. Furthermore, a dual-luciferase reporter assay identified that E2F2 was a novel direct target of miR-218 but not miR-520a in HCC. In addition, miR-218 and miR-520a were observed to negatively regulate E2F2 mRNA and protein levels. This suggested that miR-218 regulated the expression of E2F2 via directly binding to its 3′-untranslated region, whereas miR-520a affected E2F2 expression indirectly. In conclusion, these results indicated that miR-218 and miR-520a are crucial in the development of HCC via the inhibition of cell proliferation and cycle progression by downregulating E2F2.