duan, y. | bioRxiv Science

bioRxiv2025

Presence of Hepatitis B virus infection in colon cancer

Hepatitis B virus (HBV) infection affects [~]300 million people worldwide, which population is at an elevated risk of various cancers, such as gastrointestinal cancer, while the matter behind is largely unclear. In this study, we analyzed 10 colonic specimens from 6 colon cancer patients who were also chronic HBV carriers through Fluorescence-activated Cell Sorting and Immunofluorescence assay to inspect the expression of HBsAg (HBV surface antigen), NTCP (current known cellular receptor of HBV) and CD45 (common marker for immune cells) proteins in single-cell resolution. We found that presence of HBsAg in colonic cells was observed in specimens from all patients, and the proportions of HBV-infected cells were higher in tumors than normal tissues. Strikingly, HBsAg in both immune cells and NTCP-negative cells were also observed in all the patients. In vitro experiments further demonstrated that colonic cells expressing NTCP were indeed highly suspectable to HBV infection. Hence, HBV could infect colonic cells (including immune ones) and may play roles during tumorigenesis in colon cancer.

cancer biology↗

bioRxiv2019

Long noncoding RNA AVAN promotes antiviral innate immunity by interacting with TRIM25 and enhancing the transcription of FOXO3a

Accumulating evidence has shown that long noncoding RNAs (lncRNAs) are involved in several biological processes, including immune responses. However, the role of lncRNAs in antiviral innate immune responses remains largely unexplored. Here, we identify an uncharacterized human lncRNA from influenza A virus (IAV) patients, antivirus and activate neutrophil (AVAN), that is significantly up-regulated upon virus infection. Mechanistically, nuclear lncRNA-AVAN positively regulates the transcription of forkhead box O3A (FOXO3a) by associating with its promoter and inducing chromatin remodeling to promote neutrophil chemotaxis. Furthermore, we also found that cytoplasmic lncRNA-AVAN directly binds tripartite motif containing 25 (TRIM25) and enhances the association of TRIM25 and Retinoic acid inducible gene-1 proteins (RIG-I) and the ubiquitylation of RIG-I, thereby promoting TRIM25- and RIG-I-mediated antiviral innate immune signaling. More importantly, we enforced the expression of AVAN in transgenic mice and found that it significantly alleviated IAV virulence and virus production. Collectively, these findings highlight the potential clinical implications of lncRNA-AVAN as a key positive regulator of the antiviral innate immune response and a promising target for developing broad antiviral therapeutics.

immunology↗