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This paper advances a new single-parameter chaotic system with a simple structure, and some basic dynamic behavior of the new single-parameter system is discussed, such as equilibria, dissipativity, the existence of an attractor, Lyapunov exponent, Poincaré map, spectrum map, and bifurcation diagram. Moreover, a new fixed-time convergence theorem is proposed for general chaotic systems based on finite-time control theory, and a fixed-time controller is also put to achieve synchronization of the new chaotic system. Simulation results are presented to show the effectiveness of the theoretical results. The conclusion of the paper is useful for the nonlinear economics and engineering application.

The control of financial risk has always been one of the important topics in financial research. Based on the theory of finance, this paper proposes a kind of financial risk dynamic system. By analyzing some properties of the dynamic system, the system shows obvious coexisting chaotic oscillations. In order to control the financial risk dynamic system effectively, this paper proposes a finite-time impulse controller to control the financial risk dynamic system. Simulation results show that the finite-time impulse controller has faster convergence speed than the impulse controller.

This paper investigates the finite-time synchronization of complex dynamical networks with nondelayed and delayed coupling. By designing a simple continuous function controller, sufficient criteria for finite-time synchronization of dynamical networks with nondelayed and delayed coupling are obtained. As a special case, the continuous function controller designed in this paper may be the simplest and easy to implement for the finite-time synchronization of dynamical networks without delay. Finally, numerical simulations are given to verify the effectiveness of the conclusions presented in this paper.

Sen Zheng,1,* Huita Wu,2,* Fei Wang,1,* Jie Lv,1 Jing Lu,1 Qinliang Fang,1 Fuqiang Wang,1 Yuyan Lu,1 Sheng Zhang,1 Yaping Xu,3 Qing Bao,1 Chengrong Xie,1 Zhenyu Yin11Department of Hepatobiliary Surgery, Zhongshan Hospital, Xiamen University, Fujian Provincial Key Laboratory of Chronic Liver Disease and Hepatocellular Carcinoma, Xiamen 361004, Fujian, People’s Republic of China; 2Department of Oncology, Zhongshan Hospital, Xiamen University, Xiamen 361004, Fujian, People’s Republic of China; 3Key laboratory of functional and clinical translational medicine, Xiamen Medical College, Xiamen 361004, Fujian, People’s Republic of China*These authors contributed equally to this workBackground: Due to the high recurrence and metastasis rate, the clinical outcomes of patients with hepatocellular carcinoma (HCC) are still unsatisfactory. Hepatitis B virus X-interacting protein (HBXIP) has been reported to play crucial roles in carcinogenesis.Purpose: We aimed to reveal the functional significance and underlying mechanism of HBXIP in HCC metastasis.Methods: Cell transwell assay, in vivo metastasis model, real-time PCR, western blot analysis, luciferase reporter and chromatin immunoprecipitation assays were applied.Results: Here, we detected the HBXIP expression level and determined its clinical significance in HCC. We found that HBXIP was significantly upregulated in HCC tissues, and correlated with vascular invasion, tumor metastasis and worse prognosis of HCC patients. HBXIP enhanced cell migration and invasion in vitro, and promoted the metastasis of HCC in vivo. Furthermore, we confirmed that HBXIP increased MMP15 expression through association with proto-oncogene c-myc. Depletion of c-myc abolished HBXIP-mediated MMP-15 upregulation. We also observed a positive correlation between HBXIP and MMP15 expression in HCC tissues.Conclusion: Our results establish a novel function for HBXIP-MMP15 regulation in HCC metastasis and suggest its candidacy as a new prognostic biomarker and therapeutic target for HCC metastasis.Keywords: c-myc, MMP15, HBXIP, metastasis

Fei Wang,1,2 Huita Wu,3 Sheng Zhang,4 Jing Lu,1 Yuyan Lu,1 Ping Zhan,1 Qinliang Fang,1 Fuqiang Wang,1 Xiuming Zhang,5 Chengrong Xie,1 Zhenyu Yin11Department of Hepatobiliary Surgery, Fujian Provincial Key Laboratory of Chronic Liver Disease and Hepatocellular Carcinoma, Zhongshan Hospital, Xiamen University, Xiamen, Fujian, People’s Republic of China; 2The United Innovation of Mengchao Hepatobiliary Technology Key Laboratory of Fujian Province, Mengchao Hepatobiliary Hospital of Fujian Medical University, Fuzhou, Fujian, People’s Republic of China; 3Department of Oncology, Zhongshan Hospital, Xiamen University, Xiamen, Fujian, People’s Republic of China; 4Department of Pathology, Hubei Cancer Hospital, Wuhan, Hubei, People’s Republic of China; 5Department of Biomaterials, College of Materials, Xiamen University, Xiamen, Fujian, People’s Republic of ChinaBackground: Hepatocellular carcinoma (HCC) is one of the most frequent cancers and the third leading cause of cancer-related deaths. It has been reported that lysosomal associated transmembrane protein LAPTM4B expression is significantly upregulated in human cancers and closely associated with tumor initiation and progression.Purpose: We aimed to reveal the relevance of LAPTM4B and the pathogenesis of HCC. Methods: Cell viability assessment, colony formation assay, in vivo xenograrft model, microarray, real-time PCR, immunofluorescence and western blot analysis were applied.Results: Our results demonstrated that LAPTM4B promoted HCC cell proliferation in vitro and tumorigenesis in vivo. Additionally, upon starvation conditions, LAPTM4B facilitated cell survival, inhibited apoptosis and induced autophagic flux. Expression profiling coupled with gene ontology (GO) analysis revealed that 159 gene downregulated by LAPTM4B silencing was significantly enriched in response to nutrient and some metabolic processes. Moreover, LAPTM4B activated ATG3 transcription to modulate HCC cell apoptosis and autophagy.Conclusion:Our findings demonstrate that LAPTM4B acts as an oncogene that promotes HCC tumorigenesis and autophagy, and indicate that LAPTM4B may be used as a novel therapeutic target for HCC treatment.Keywords: autophagy, apoptosis, LAPTM4B, ATG3