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As a security issue, privacy protection has been widely valued in the security field. Based on privacy protection, this brief discusses the finite-time (FnT) synchronization of complex networks. Firstly, the FnT convergence theorem for dynamical systems is discussed. Secondly, FnT privacy protection function (PPF) is designed, the main idea of this method is to propose a FnT privacy protection function which can cover up the real state of the controlled complex network, that is, in a FnT, instead of transmitting their actual state values, the controlled network acts on the values of the design function. The designed function is continuous time-varying functions that converge to the true state in FnT. Finally, simulations mean that the proposed design method is effective.

ABSTRACTLong non-coding RNAs are essential to hepatocellular carcinoma (HCC) development, progression, and incidence of drug resistance. However, the biological significance of long non-coding RNA muskelin 1 antisense RNA (MKLN1-AS) remains poorly characterized. In this study, we observed noticeable increased levels of MKLN1-AS in HCC tissues. This upregulation of MKLN1-AS was clinically associated with vascular invasion and decreased disease-free survival and overall survival of patients with HCC. Functionally, MKLN1-AS-knockdown dramatically suppressed the metastasis and growth of HCC cells in vitroand in vivo. Additionally, the knockdown of MKLN1-AS augmented the pro-apoptosis effect of lenvatinib. Taken together, our findings indicate that MKLN1-AS may be exploited as a potential prognostic predictor and therapeutic target for HCC treatment.

Ubiquitin-specific protease 11 (USP11) is a deubiquitinating enzyme that exerts its biological functions by regulating multiple signaling pathways such as p53, NF-κB, TGF-β, and Hippo. A large body of evidence supports a link between UPS11 and tumorigenesis. However, the clinical significance and biological function of USP11 in hepatocellular carcinoma (HCC) remains unclear. Here, USP11 expression was assessed by immunohistochemistry in a pilot series of 71 HCC clinical samples, and the association between USP11 expression and clinicopathological features and overall survival time was analyzed. The cytoplasmic expression rate of USP11 was higher in non-cancerous tissue than that in cancer tissue (36.6 vs. 12.7%, P= 0.001), whereas the nuclear expression rate of USP11 was lower in non-cancerous tissue (5.6 vs. 69.0%, P< 0.001). USP11 expression level was higher in tumor than that in non-tumor tissue (P< 0.001). Chi-square analysis of variances suggested that USP11 expression was associated with vascular invasion (P= 0.033), differentiation (P= 0.027), tumor number (P= 0.009), and recurrence (P= 0.036). USP11 expression was also associated with shorter overall survival time (P= 0.001) by log-rank test. Unconditional logistic regression analysis with multiple covariates indicated that high USP11 expression was associated with a 2.96-fold increase in the risk of death compared with low USP11 levels (P= 0.041) and acted as an independent predictor of overall survival. HCC patients with simultaneously high USP11 and alpha-fetoprotein expression had an adjusted 5-fold higher risk of all-cause-related death (P= 0.006). Moreover, in vitro and in vivo experiments confirmed that USP11 could promote the migration and invasion of HCC cell. Overall, we suggest that USP11 promotes HCC cell metastasis, and we provide the first evidence of the prognostic significance of USP11 expression in HCC, which suggests that USP11 is a promising therapeutic target for the treatment of HCC.

Ubiquitin-specific protease 11 (USP11) is a deubiquitinating enzyme that exerts its biological functions by regulating multiple signaling pathways such as p53, NF-κB, TGF-β, and Hippo. A large body of evidence supports a link between UPS11 and tumorigenesis. However, the clinical significance and biological function of USP11 in hepatocellular carcinoma (HCC) remains unclear. Here, USP11 expression was assessed by immunohistochemistry in a pilot series of 71 HCC clinical samples, and the association between USP11 expression and clinicopathological features and overall survival time was analyzed. The cytoplasmic expression rate of USP11 was higher in non-cancerous tissue than that in cancer tissue (36.6 vs. 12.7%, P= 0.001), whereas the nuclear expression rate of USP11 was lower in non-cancerous tissue (5.6 vs. 69.0%, P< 0.001). USP11 expression level was higher in tumor than that in non-tumor tissue (P< 0.001). Chi-square analysis of variances suggested that USP11 expression was associated with vascular invasion (P= 0.033), differentiation (P= 0.027), tumor number (P= 0.009), and recurrence (P= 0.036). USP11 expression was also associated with shorter overall survival time (P= 0.001) by log-rank test. Unconditional logistic regression analysis with multiple covariates indicated that high USP11 expression was associated with a 2.96-fold increase in the risk of death compared with low USP11 levels (P= 0.041) and acted as an independent predictor of overall survival. HCC patients with simultaneously high USP11 and alpha-fetoprotein expression had an adjusted 5-fold higher risk of all-cause-related death (P= 0.006). Moreover, in vitro and in vivo experiments confirmed that USP11 could promote the migration and invasion of HCC cell. Overall, we suggest that USP11 promotes HCC cell metastasis, and we provide the first evidence of the prognostic significance of USP11 expression in HCC, which suggests that USP11 is a promising therapeutic target for the treatment of HCC.