Speakers - 2025

Biography

Dr. Peng Ruan is an Associate Chief Physician specializing in Gastroenterology at Renmin Hospital of Wuhan University, China. With a Ph.D. in internal medicine from Wuhan University, he brings extensive expertise in hepatology. Dr. Ruan's diverse professional journey includes roles as a resident physician in General Internal Medicine and ICU, as well as leadership positions in gastroenterology. He has also served as a visiting scholar at INSERM U1052, Université Claude Bernard, Lyon, France. Dr. Ruan's research focus encompasses the study of chimeric protein transcription of HBV integration sites and the detection of intrahepatic HBV cccDNA in chronic hepatitis B patients. His contributions have been supported by grants from the National Natural Science Fund of Hubei Province and the Shiyan Science Technology and Innovation Committee.

Abstract

Hepatitis B virus (HBV) integration into the human genome causes hepatocellular carcinoma (HCC). The present study used inverse nested PCR; the full sequence of HBV DNA fragments of the chrX: 111009033 integration site was detected (987 bp), containing two fragments of double-stranded linear DNA with the same orientation (1,744-1,094 and 1,565-1,228 nt). By reverse transcription‑quantitative PCR, HBV‑cell fusion transcript was observed in HepG2.2.15 cells. The mean copy number of this site in cells with H₂O₂ treatment (8.73x10⁻²±1.65x10⁻² copies/cell) was significantly higher than that in the cells without H₂O₂ treatment (3.02x10⁻²±2.33x10⁻² copies/cell; P<0.0001). The mean levels of P21‑activated kinase 3 (PAK3) were 15.67±5.65 copies/cell in HepG2.2.15 cells with H₂O₂ treatment, significantly higher than in the cells without H₂O₂ treatment (11.34±4.58 copies/cell, P=0.0076) and in HepG2 cells (5.92±1.54 copies/cell, P<0.0001). A significant difference in PAK3 levels was also found between HepG2.2.15 cells without H₂O₂ treatment and HepG2 cells (11.34±4.58 vs. 5.92±1.54 copies/cell, P<0.0001). The average copy numbers of the integration site chrX: 111009033 were positively correlated with the average levels of PAK3 (P=0.0013). The overall trend of PAK3 expression was significantly increased in HepG2. 2.15 cells with H₂O₂ treatment compared with that in HepG2. 2.15 cells without H₂O₂ treatment (37.63±8.16 and 31.38±7.94, P=0.008) and HepG2 cells (21.67±7.88, P<0.0001). In summary, the chrX: 11009033 integration site may originate from primary human hepatocytes, the occurrence and clonal expansion of which may upregulate PAK3 expression, which may contribute to hepatocarcinogenesis.