ArticleInternational journal of oncology2019
SIP1 serves a role in HBx‑induced liver cancer growth and metastasis.
Article in International journal of oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Roles of X-box binding protein 1 in liver pathogenesis.Clinical and molecular hepatology · 2025Review
- Role of hepatitis B virus non-structural protein HBx on HBV replication, interferon signaling, and hepatocarcinogenesis.Frontiers in microbiology · 2023Review
- Review
- Hepatitis B virus X protein mediated epigenetic alterations in the pathogenesis of hepatocellular carcinoma.Hepatology international · 2022Review
- The pathogenesis of liver cancer and the therapeutic potential of bioactive substances.Frontiers in pharmacology · 2022Review
- Downregulation of HBx Restrains Proliferation, Migration, and Invasion of HepG2 Cells.Analytical cellular pathology (Amsterdam) · 2021Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus (HBV) has been revealed to be involved in the development of hepatocellular carcinoma. However, the mechanism remains to be fully elucidated. Smad‑interacting protein 1 (SIP1) is a transcriptional repressor, which serves a pivotal role in cell metastasis. In the present study, the role of SIP1 in HBx‑induced hepatocyte EMT and cancer aggressiveness was examined. It was found that HBV X protein (HBx) increased the expression of SIP1 and recruited it to the promoter of E‑cadherin, resulting in depression of the transcription of E‑cadherin. Histone deacetylase 1 was also found to be involved in the repressive complex formation. Furthermore, in an orthotopic tumor transplantation model in vivo, HBx promoted tumor growth and metastasis, whereas the knockdown of SIP1 attenuated the effect of HBx. These results indicate a novel mechanism for the development of HBV‑related liver cancer.
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