HYBRID EVENT: You can participate in person at Paris, France or Virtually from your home or work.

6th Edition of World Congress on Infectious Diseases

June 24-26, 2024 | Paris, France

June 24 -26, 2024 | Paris, France
Infection 2022

Kai-Fu Tang

Speaker at Infection Conferences - Kai-Fu Tang
Chongqing Medical University, China
Title : Role of Dicer in the pathogenesis of HBV-associated hepatocellular carcinoma


Dicer, a key component of the RNA interference pathway, is also essential for DNA repair. Reactive oxygen species in inflamed liver tissues induce DNA damage and decrease Dicer expression. The downregulation of Dicer, in turn, reduces DNA repair efficiency and leads to increased DNA damage. DNA damage leads to an aggravation of inflammation via various mechanisms. First, it induces the expression of the natural killer group 2D (NKG2D) receptor ligands, and the binding of these ligands to their receptor promotes inflammation. Second, DNA damage promotes the release of nuclear DNA into the cytoplasm. Consequently, the cytosolic DNA sensing machinery induces the secretion of proinflammatory cytokines. Thus, decreased Dicer expression plays a central role in the development of unresolved chronic inflammation, a common and important factor in neoplasia pathogenesis. In addition to promoting inflammation, decreased Dicer expression may promote the development of hepatocellular carcinoma via the following mechanisms. First, decreased Dicer expression reduces DNA repair efficiency, promoting gene mutation and eventually carcinogenesis. Second, Dicer processes 7SL RNA into small fragments that function as dominant negative regulators of the full-length 7SL RNA and interfere with signal recognition particle (SRP) complex formation. Accordingly, a decrease in Dicer expression promotes SRP complex formation via a downregulation of the 7SL RNA fragment biogenesis, which then enhances SRP-mediated protein targeting and increases the translocation and expression of membrane and secretory proteins, which are upregulated in tumor tissues. Finally, decreased Dicer expression may promote carcinogenesis by deregulating miRNA expression.


Dr. Kai-Fu Tang graduated from Chongqing Medical University, Peking Union Medical College, and Chongqing University with a Bachelor’s degree in Medicine, a Master of science degree, and a Doctoral degree in Engineering, respectively. He has successively worked in Huaying People's Hospital (Sichuan, China), University of Cologne (Cologne, Germany), Friedrich Miescher Institute (Basel, Switzerland), Second Affiliated Hospital of Chongqing Medical University (Chongqing, China), Wenzhou Medical University (Wenzhou, China), The First Affiliated Hospital of Medical University (Wenzhou, China), and Chongqing Medical University (Chongqing, China). Currently, Dr. Tang is a professor at the Key Laboratory of Molecular Biology on Infectious Diseases, Ministry of Education, Chongqing Medical University. Dr. Tang's research is focused on the role of Dicer in inflammation and inflammation-driven carcinogenesis. He has published more than 30 papers in international journals such as Genome Biol, J Cell Biol, Nucleic Acids Res, Oncogene, Cell Rep, Theranostics, Pharmacol Res, Cell Death Dis, Carcinogenesis, and J Biol Chem.