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Editor | xi Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide.
A variety of pathological factors, such as HBV and HCV infection, alcohol consumption, oncogene DNA damage, and obesity, can induce the inflammatory tumor microenvironment, thereby promoting the occurrence and development of liver cancer.
On May 25, 2021, Professor Sun Beicheng of Drum Tower Hospital Affiliated to Nanjing University School of Medicine and Dr.
Lin Anning, a dual-appointed professor at Nanjing University Institute of Modern Biology and Drum Tower Hospital (Drum Tower Hospital, Nanjing University School of Medicine, Deputy Chief Physician Zhang Wenjie, PhD student Zhang Yuan Guangyan and Wang Fei as the first authors) published an article The zinc finger protein Miz1 suppresses liver tumorigenesis by restricting hepatocyte-driven macrophage activation and inflammation in Immunity, revealing a new mechanism for the regulation of liver cancer transformation.
The results of the research team of Sun Beicheng and Lin Anning proved that abnormal liver cell NF-κB activity, whether it is missing or increased, can induce inflammatory tumor microenvironment through different molecular mechanisms, thereby promoting the occurrence and development of liver cancer.
Two different mouse liver cancer models induced by chemical DEN/CCl4 and inflammatory-mediated STZ/HFD were used to deeply analyze the interaction between liver cancer cells and macrophages in the liver cancer microenvironment through single-cell sequencing, and found mouse liver cells The lack of the transcription factor Miz1 produces a specific “inflammatory” hepatocyte subpopulation that highly expresses NF-κB downstream inflammatory factors, activates tumor-infiltrating macrophages to transform into a pro-inflammatory phenotype, enhances liver inflammation, and promotes the occurrence of liver cancer development of.
Mechanism studies have found that the Miz1 protein in the cytoplasm of liver cells is regulated by proteolysis induced by tumor necrosis factor TNF, and is induced to down-regulate in the process of human/mouse liver cancer, thereby releasing the oncoprotein MTDH bound to Miz1 and enhancing the protein kinase IKK Phosphorylation of MTDH promotes the activation of NF-κB and the expression of downstream inflammatory factors in liver cells.
Interestingly, this mechanism of Miz1 does not depend on the function of its transcription factors.
In a considerable part of clinical liver cancer patients, the low expression of Miz1 in liver cancer tissues is accompanied by an increase in phosphorylation of MTDH and an increase in hepatocytes secreting inflammatory factors.
At the same time, the expression of Miz1 protein has also been confirmed to be closely related to the survival rate and recurrence rate of liver cancer patients, and is an independent prognostic related factor.
Based on multi-omics analysis, this study used a variety of in vivo and in vitro experiments to reveal the specific mechanism by which Miz1 protein deletion in liver cells activates NF-κB and enhances inflammation through MTDH during the development of liver cancer, and proposes the liver as the main body of liver tumors.
The important hypothesis that cells drive cancer-promoting inflammation provides a new target for personalized treatment of liver cancer patients.
The work was jointly completed by researchers from the Gulou Hospital Affiliated to the School of Medicine of Nanjing University, the Institute of Modern Biology, Nanjing University, the University of Chicago, and the Institute of Biochemistry and Cell Biology of the Chinese Academy of Sciences.
The Hepatobiliary and Pancreatic Center of Gulou Hospital is mainly engaged in the research of liver cancer immune microenvironment, liver surgery and liver transplantation.
The subject leader is Professor Sun Beicheng.
Talents at home and abroad are welcome to join.
Original link: https://doi.
org/10.
1016/j.
immuni.
2021.
04.
027 Plate maker: Notes for reprinting on the 11th [Non-original article] The copyright of this article belongs to the author of the article.
Personal forwarding and sharing are welcome.
Reprinting is prohibited without permission.
The author has all legal rights, and offenders must be investigated.
A variety of pathological factors, such as HBV and HCV infection, alcohol consumption, oncogene DNA damage, and obesity, can induce the inflammatory tumor microenvironment, thereby promoting the occurrence and development of liver cancer.
On May 25, 2021, Professor Sun Beicheng of Drum Tower Hospital Affiliated to Nanjing University School of Medicine and Dr.
Lin Anning, a dual-appointed professor at Nanjing University Institute of Modern Biology and Drum Tower Hospital (Drum Tower Hospital, Nanjing University School of Medicine, Deputy Chief Physician Zhang Wenjie, PhD student Zhang Yuan Guangyan and Wang Fei as the first authors) published an article The zinc finger protein Miz1 suppresses liver tumorigenesis by restricting hepatocyte-driven macrophage activation and inflammation in Immunity, revealing a new mechanism for the regulation of liver cancer transformation.
The results of the research team of Sun Beicheng and Lin Anning proved that abnormal liver cell NF-κB activity, whether it is missing or increased, can induce inflammatory tumor microenvironment through different molecular mechanisms, thereby promoting the occurrence and development of liver cancer.
Two different mouse liver cancer models induced by chemical DEN/CCl4 and inflammatory-mediated STZ/HFD were used to deeply analyze the interaction between liver cancer cells and macrophages in the liver cancer microenvironment through single-cell sequencing, and found mouse liver cells The lack of the transcription factor Miz1 produces a specific “inflammatory” hepatocyte subpopulation that highly expresses NF-κB downstream inflammatory factors, activates tumor-infiltrating macrophages to transform into a pro-inflammatory phenotype, enhances liver inflammation, and promotes the occurrence of liver cancer development of.
Mechanism studies have found that the Miz1 protein in the cytoplasm of liver cells is regulated by proteolysis induced by tumor necrosis factor TNF, and is induced to down-regulate in the process of human/mouse liver cancer, thereby releasing the oncoprotein MTDH bound to Miz1 and enhancing the protein kinase IKK Phosphorylation of MTDH promotes the activation of NF-κB and the expression of downstream inflammatory factors in liver cells.
Interestingly, this mechanism of Miz1 does not depend on the function of its transcription factors.
In a considerable part of clinical liver cancer patients, the low expression of Miz1 in liver cancer tissues is accompanied by an increase in phosphorylation of MTDH and an increase in hepatocytes secreting inflammatory factors.
At the same time, the expression of Miz1 protein has also been confirmed to be closely related to the survival rate and recurrence rate of liver cancer patients, and is an independent prognostic related factor.
Based on multi-omics analysis, this study used a variety of in vivo and in vitro experiments to reveal the specific mechanism by which Miz1 protein deletion in liver cells activates NF-κB and enhances inflammation through MTDH during the development of liver cancer, and proposes the liver as the main body of liver tumors.
The important hypothesis that cells drive cancer-promoting inflammation provides a new target for personalized treatment of liver cancer patients.
The work was jointly completed by researchers from the Gulou Hospital Affiliated to the School of Medicine of Nanjing University, the Institute of Modern Biology, Nanjing University, the University of Chicago, and the Institute of Biochemistry and Cell Biology of the Chinese Academy of Sciences.
The Hepatobiliary and Pancreatic Center of Gulou Hospital is mainly engaged in the research of liver cancer immune microenvironment, liver surgery and liver transplantation.
The subject leader is Professor Sun Beicheng.
Talents at home and abroad are welcome to join.
Original link: https://doi.
org/10.
1016/j.
immuni.
2021.
04.
027 Plate maker: Notes for reprinting on the 11th [Non-original article] The copyright of this article belongs to the author of the article.
Personal forwarding and sharing are welcome.
Reprinting is prohibited without permission.
The author has all legal rights, and offenders must be investigated.
