Characterization of Group Behavior of Corruption in Construction Projects Based on Contagion Mechanism.

With the rapid development of construction projects, more and more engineering corruption problems have emerged. Therefore, this paper proposes a SEIR (susceptible-exposed-infected-recovered) based corruption model to better understand the propagation process of corruption cases in construction projects. In this model, the data samples are collected from the 2018 Engineering Corruption Case Judgment Document, the propagation parameters are obtained through actual case analysis with the help of complex networks, the change process and key influencing factors of actual nodes in engineering corruption cases are simulated by Python. The study results indicate that the personnel conforms to the "4-9 transmission law," in which the early stage is a period of high incidence of corruption cases. The network of corruption cases is somewhat vulnerable, and its spread is about minus 8 times the change in crackdown rate and 10 times the change in infection rate. The variation range of the susceptible population S and the removed person R in the propagation simulation curve can predict the relationship between corruption infection rate and crackdown rate, which can provide theoretical guidance for preventing the occurrence of corruption.

Long noncoding RNA lncTCF7, induced by IL-6/STAT3 transactivation, promotes hepatocellular carcinoma aggressiveness through epithelial-mesenchymal transition.

BACKGROUND: Accumulating evidence suggests the pro-inflammatory cytokine interleukin-6 (IL-6) in tumor microenvironment may promote the development of hepatocellular carcinoma (HCC). However, the underlying mechanism remains largely unknown. METHODS: The expression and promoter activity of lncTCF7 were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and luciferase reporter assay. The function of the STAT3 binding site in the lncTCF7 promoter region was tested by luciferase reporter assay with nucleotide substitutions. The binding of STAT3 to the lncTCF7 promoter was confirmed by chromatin immunoprecipitation assay (CHIP) in vivo. The effects of decreasing STAT3 with small interference RNA and inhibiting STAT3 activation by small molecular inhibitor on lncTCF7 expression were also determined. RESULTS: We demonstrate that IL-6 could induce lncTCF7 expression in a time- and dose-dependent manner, and we showed that IL-6 transcriptionally activated the expression of lncTCF7 in HCC cells by activating STAT3, a transcription activator which binds to promoter regions of lncTCF7. Furthermore, knocking-down STAT3 and inhibiting STAT3 activation reduced lncTCF7 expression. Importantly, RNA interference-based attenuation of lncTCF7 prevented IL-6-induced EMT and cell invasion. CONCLUSION: Thus, these data provides evidence to the existence of an aberrant IL-6/STAT3/ lncTCF7 signaling axis that leads to HCC aggressiveness through EMT induction, which could be novel therapeutic targets in malignancies.