DNA immune recognition regulation mediated by the cGAS-STING pathway plays an important role in immune functions. Under normal physiological conditions, cGAS can recognize and bind to invading pathogen DNA and activate the innate immune response. On the other hand, abnormal activation of cGAS or STING is closely related to autoimmune diseases. In addition, activation of STING proteins as a bridge connecting innate immunity and adaptive immunity can effectively restrain tumor growth. Therefore, targeting the cGAS-STING pathway can alleviate autoimmune symptoms and be a potential drug target for treating cancer. This article summarizes the current progress on cGAS-STING pathway modulators and lays the foundation for further investigating therapeutic development in autoimmune diseases and tumors.
Role of circ-FNTA in the progression of bladder cancer (BCa) and its underlying mechanism were investigated. circ-FNTA level in BCa tissues and cell lines was detected. The prognostic potential of circ-FNTA was assessed by Kaplan-Meier methods and the proliferative and invasive abilities of BCa influenced by circ-FNTA were explored. Through dual-luciferase reporter gene assay, miRNA-451a, the target of circ-FNTA and the target gene of miRNA-451a, S1PR3 were determined. circ-FNTA was upregulated in BCa, especially in invasive BCa. High level of circ-FNTA indicated worse prognosis in BCa patients. Silence of circ-FNTA attenuated the proliferative and invasive abilities of T24 and UM-UC-3 cells. miRNA-451a was verified to be the target of circ-FNTA, which was downregulated in BCa cells. circ-FNTA negatively regulated the expression level of miRNA-451a. Moreover, S1PR3 was the downstream gene of miRNA-451a. Overexpression of miRNA-451a downregulated S1PR3 level in BCa cells. circ-FNTA accelerates the proliferative and invasive abilities of BCa through targeting miRNA-451a/S1PR3 axis, and indicates a poor prognosis of BCa patients.
IFNβ is a single-copy gene without an intron. Under normal circumstances, it shows low or no expression in cells. It is upregulated only when the body needs it or is stimulated. Stimuli bind to the pattern recognition receptors (PRRs) and pass via various signaling pathways to several basic transcriptional regulators, such as IRFs, NF-кB, and AP-1. Subsequently, the transcriptional regulators enter the nucleus and bind to regulatory elements of the IFNβ promoter. After various modifications, the position of the nucleosome is altered and the complex is assembled to activate the IFNβ expression. However, IFNβ regulation involves a complex network. For the study of immunity and diseases, it is important to understand how transcription factors bind to regulatory elements through specific forms, which elements in cells are involved in regulation, what regulation occurs during the assembly of enhancers and transcription complexes, and the possible regulatory mechanisms after transcription. Thus, this review focuses on the various regulatory mechanisms and elements involved in the activation of IFNβ expression. In addition, we discuss the impact of this regulation in biology.
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