A new molecular mechanism of complex interaction between viral infection and tumor.

On January 16th, the latest research from the Institute of Excellence in Molecular Cell Science of the Chinese Academy of Sciences/Institute of Biochemistry and Cell Biology, Zhou Zhaocai Research Group, was published online in The Journal of The Journal of TheRapy Again saperssatEd Agains GastriCancer Cancer.
this study reveals the regulatory effect of antiviral signaling pathways on Hippo signaling pathways, especially the regulatory mechanism of IRF3 to enhance YAP activity, and finds that IRF3 can be used as a therapeutic target for YAP high-expression gastric cancer, providing a basis for exploring the lesions mechanism of gastric cancer and the research and development of related drug screening and diagnosis and treatment strategies.
Hippo signaling pathway seiswells play a key role in the development of biological individuals, especially in the process of tissue size regulation, and play an important role in tumor occurrence and immune response.
Zhou Zhaocai research group is committed to the study of tumor occurrence and immune response of molecular cell signaling mechanism, a series of recent work revealed hippo, TLR and other signaling pathways in gastrointestinal malignancies and inflammatory immune response in the mechanism and function, found a number of new disease diagnosis and treatment markers and drug targets.
researchers analyzed the clinical samples of gastric cancer patients to clarify that IRF3 expression showed a significant upward trend in tumors and was significantly positively correlated with the expression of YAP.
further combined with research techniques such as ChIP-Seq and RNA-Seq, it was found that viral stimulation can significantly promote YAP activity and transcription of downstream genes.
mechanism, after IRF3 phosphate into the nucleus, it can form a complex with YAP and TEAD, maintain intranuclear protein levels, stabilize the combination of YAP-TEAD and target genes, and promote the proliferation of gastric cancer cells (see figure).
cell and mouse gastric cancer models show that knocking out IRF3 or using small molecular compounds to inhibit IRF3 activity can block THE growth of YAP-driven stomach cancer.
study reveals a new molecular mechanism of complex interaction between viral infection and tumor, clarifies the pathological correlation between IRF3, the key antiviral molecule, and the key molecule of tumor proliferation, suggests that IRF3 can be used as a new drug target and provides new ideas for the treatment of gastric cancer and other malignant tumors with high YAP level.
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