Bufalin inhibits hepatitis B virus-associated hepatocellular carcinoma development through androgen receptor dephosphorylation and cell cycle-related kinase degradation
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Purpose Hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC), which has a male predominance, lacks effective therapeutic options. Previously, the cardiac glycoside analogue bufalin has been found to inhibit HBV infection and HCC development. As yet, however, its molecular role in HBV-associated HCC has remained obscure. Methods Colony formation and soft agar assays, xenograft and orthotopic mouse models and HBV X protein (HBx) transgenic mice with exposure to diethylnitrosamine were used to evaluate the effect of bufalin on HBV-associated HCC growth and tumorigenicity. HBx-induced oncogenic signaling regulated by bufalin was assessed using PCR array, chromatin immunoprecipitation, site-directed mutagenesis, luciferase reporter, transcription and protein expression assays. Synergistic HCC therapeutic effects were examined using combinations of bufalin and sorafenib. Results We found that bufalin exerted a more profound effect on inhibiting the proliferation of HBV-associated HCC cells than of non HBV-associated HCC cells. Bufalin significantly inhibited HBx-induced malignant transfromation in vitro and tumorigenicity in vivo. Androgen receptor (AR) signaling was found to be a target of bufalin resistance to HBV-associated hepatocarcinogenesis. We also found that bufalin induced both AR dephosphorylation and cell cycle-related kinase (CCRK) degradation to inhibit β-catenin/TCF signaling, which subsequently led to cell cycle arrest via cyclin D1 down-regulation and…
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Bufalin has been previously reported to associate with mTOR and AR.
“Given that the association of Bufalin with mTOR and AR has been previously reported26,27, we evaluated the binding of Bufalin to recombinant human ESR1, PRKCD, and CYP17A1 proteins using surface plasmon resonance (SPR) assays.”
From Harnessing artificial intelligence to identify Bufalin as a molecular glue degrader of estrogen receptor alpha (2025) · cites this paper as [27]
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- Authors
- Yu, Z., Feng, H., Zhuo, Y., Li, M., Zhu, X., Huang, L., Zhang, X., Zhou, Z., Zheng, C., Jiang, Y., Le, F., Yu, D.-Y., Cheng, A. S., Sun, X., & Gao, Y.
- Affiliations
- Shanghai University of Traditional Chinese Medicine (CN)
- Harbin Medical University (CN)
- Korea Research Institute of Bioscience and Biotechnology (KR)
- Chinese University of Hong Kong (HK)
- Corresponding author
- Yu, Zhuo
- Sun, Xuehua
- Gao, Yueqiu
- ORCID
- Venue
- Cellular Oncology
- Published
- 2020-07-04
- Volume
- 43
- Issue
- 6
- Pages
- 1129-1145
- ISSN
- 1570-5870 (ISSN-L)
- 2211-3428
- 2211-3436
- PMC
- PMC12990746
- OpenAlex
- W3040461816
- Cited by
- 27
- References
- 52
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 3 · 2023: 8 · 2022: 8 · 2021: 1
- FWCI
- 2.65
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Cellular Oncology (publishedVersion, cc-by)
- PubMed (publishedVersion)
- PubMed Central (publishedVersion)
- Funders
- National Natural Science Foundation of China (81774240, 81673935, 81672789, 81673938)
- Chenguang Program from Shanghai Education Development Foundation and Shanghai Municipal Education Commission (15CG48)
- Shanghai Rising-Star Program (17QA1403900)
- Training plan of outstanding young medical talents, Shanghai Municipal Health Bureau (2017YQ021)
- Scientific and technological project supported by Shanghai Municipal Science and Technology Commission (16401970600)
- Topics
- Health Sciences › Medicine › Hepatology › Hepatocellular Carcinoma Treatment and Prognosis
- Health Sciences › Medicine › Epidemiology › Hepatitis B Virus Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Keywords
- bufalin, beta-catenin/TCF signaling, cyclin D1, p21, cell cycle arrest, sorafenib combination therapy, diethylnitrosamine-induced hepatocarcinogenesis, cardiac glycosides
- MeSH terms
- Glycogen Synthase Kinase 3 beta, Sorafenib, Cyclin-Dependent Kinase-Activating Kinase, Animals, Bufanolides, Hepatitis B virus, Carcinoma, Hepatocellular, Liver Neoplasms, Mice, Nude, Mice, Transgenic, Models, Biological, Phosphorylation, Receptors, Androgen, Signal Transduction, Trans-Activators, Cyclin-Dependent Kinases, Cell Line, Tumor, Cell Proliferation, beta Catenin, Viral Regulatory and Accessory Proteins, Cell Cycle Checkpoints, Proteolysis, Carcinogenesis
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