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Updated: Apr 5, 2026

Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells
Published on: June 5, 2020
Hepatitis B virus X protein modifies invasion, proliferation and the inflammatory response in an HTR-8/SVneo cell
Hong Cui1, Qiu-Ling Li1, Jing Chen1
1Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Abstract:
Mother-to-infant transmission of hepatitis B virus (HBV) can occur as an intrauterine, intrapartum or postpartum infection. In the present study, we induced a multifunctional viral regulator of HBV gene products, HBx, and its different fragments to overexpress in a tropho-blast cell line, HTR-8/SVneo. We then identified the biological effects of HBx on HTR-8/SVneo cells. Our results indicated that HBx inhibited apoptosis and induced invasion as detected using Annexin V/propidium iodide (PI) double staining and Transwell assay, respectively. Furthermore, we carried out western blot analysis to analyze the possible related signaling pathway. We confirmed that HBx and its different fragments can activate the Smad signaling pathway, accompanied by downregulation of E-cadherin, and upregulation of vimentin and N-cadherin. TGF‑β1 was used as a control to activate the Smad signaling pathway in HTR-8/SVneo cells. HBx activated the Smad signaling pathway in the HTR-8/SVneo cells. After the signaling pathway was activated, reduced apoptosis, higher invasive ability and enhanced inflammatory response were observed in the HTR-8/SVneo cells.
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