ArticleCell cycle (Georgetown, Tex.)2012
Interaction between ZBP-89 and p53 mutants and its contribution to effects of HDACi on hepatocellular carcinoma.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 25 citations in OpenAlex.
- Unravelling butyrate metabolism in sepsis: identification of key genes.BMC infectious diseases · 2025Article
- p63 and ZNF148 cooperate to regulate head and neck squamous cell carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A study on construction of a prognosis model for liver cancer based on analgesic targets and screening therapeutic drugs.Genes & genomics · 2024Article
- Identification and validation of three core genes in p53 signaling pathway in hepatitis B virus-related hepatocellular carcinoma.World journal of surgical oncology · 2021Article
- SPAG5 interacts with CEP55 and exerts oncogenic activities via PI3K/AKT pathway in hepatocellular carcinoma.Molecular cancer · 2018Article
- Mcl-1 as a potential therapeutic target for human hepatocelluar carcinoma.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2016Article
- ZBP-89 reduces histone deacetylase 3 by degrading IkappaB in the presence of Pin1.Journal of translational medicine · 2015Article
- Epigenetic upregulation of Bak by ZBP-89 inhibits the growth of hepatocellular carcinoma.Biochimica et biophysica acta · 2013Article
- Histone deacetylase inhibitors facilitate dihydroartemisinin-induced apoptosis in liver cancer in vitro and in vivo.PloS one · 2012Article
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Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
Abstract
ZBP-89, a zinc finger transcription factor, participates in histone deacetylases inhibitors (HDACi)-mediated growth arrest and apoptosis in cancer cells. p53 mutants may interact with ZBP-89 that transcriptionally regulates p21(Waf1) (p21). However, this interaction and its consequence in cancer treatments are poorly understood. In this study, we demonstrate that ZBP‑89 is essentially required in HDACi-mediated p21 upregulation in hepetocellular carcinoma (HCC). Overexpression of ZBP-89 protein enhanced the lethal effectiveness of Trichostatin A (TSA). p53 mutant p53(G245D), but not p53(R249S), directly bound to ZBP-89 and prevented its translocation from cytoplasm to nucleus. Furthermore, p53(G245D) was shown to have a similar pattern of subcellular localization to ZBP-89 in tissues of HCC patients in Hong Kong. Functionally, the cytoplasmic accumulation of ZBP-89 by p53(G245D) significantly abrogated the induction of p21 caused by sodium butyrate (NaB) treatment and protected cells from TSA-induced death. The activations of several apoptotic proteins, such as Bid and PARP, were involved in p53(G245D)-mediated protection. Moreover, the resistance to HDACi in p53(G245D)-expressing cells was reversed by overexpression of ZBP-89. Taken together, these data suggest a potential mechanism via which mutant p53 enables tumor cells to resist chemotherapy and, therefore, establish a plausible link between mutant p53 binding to ZBP-89 and a decreased chemosensitivity of HCC cells.
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