دورية أكاديمية
أعرض في EDS

Interaction between ZBP-89 and p53 mutants and its contribution to effects of HDACi on hepatocellular carcinoma.

التفاصيل البيبلوغرافية
العنوان: Interaction between ZBP-89 and p53 mutants and its contribution to effects of HDACi on hepatocellular carcinoma.
المؤلفون: Zhang CZ; Department of Surgery, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, NT Hong Kong., Chen GG, Merchant JL, Lai PB
المصدر: Cell cycle (Georgetown, Tex.) [Cell Cycle] 2012 Jan 15; Vol. 11 (2), pp. 322-34. Date of Electronic Publication: 2012 Jan 15.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Taylor & Francis Country of Publication: United States NLM ID: 101137841 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1551-4005 (Electronic) Linking ISSN: 15514005 NLM ISO Abbreviation: Cell Cycle Subsets: MEDLINE
أسماء مطبوعة: Publication: 2015- : Philadelphia, PA : Taylor & Francis
Original Publication: Georgetown, TX : Landes Bioscience, c2002-
مواضيع طبية MeSH: Antineoplastic Agents/*pharmacology , Butyrates/*pharmacology , Carcinoma, Hepatocellular/*metabolism , DNA-Binding Proteins/*metabolism , Histone Deacetylase Inhibitors/*pharmacology , Hydroxamic Acids/*pharmacology , Mutant Proteins/*metabolism , Transcription Factors/*metabolism , Tumor Suppressor Protein p53/*metabolism, Apoptosis ; Carcinoma, Hepatocellular/genetics ; Cell Line, Tumor/drug effects ; Cell Survival/drug effects ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; DNA-Binding Proteins/genetics ; Drug Resistance, Neoplasm ; G1 Phase Cell Cycle Checkpoints/drug effects ; Gene Expression ; Humans ; Mutant Proteins/genetics ; Mutation, Missense ; Protein Binding ; Transcription Factors/genetics ; Tumor Suppressor Protein p53/genetics
مستخلص: 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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معلومات مُعتمدة: R01 DK055732 United States DK NIDDK NIH HHS; R01-DK055732 United States DK NIDDK NIH HHS
المشرفين على المادة: 0 (Antineoplastic Agents)
0 (Butyrates)
0 (Cyclin-Dependent Kinase Inhibitor p21)
0 (DNA-Binding Proteins)
0 (Histone Deacetylase Inhibitors)
0 (Hydroxamic Acids)
0 (Mutant Proteins)
0 (TP53 protein, human)
0 (Transcription Factors)
0 (Tumor Suppressor Protein p53)
0 (ZNF148 protein, human)
3X2S926L3Z (trichostatin A)
تواريخ الأحداث: Date Created: 20120105 Date Completed: 20120830 Latest Revision: 20211021
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC3293381
DOI: 10.4161/cc.11.2.18758
PMID: 22214764
قاعدة البيانات: MEDLINE
الوصف
تدمد:1551-4005
DOI:10.4161/cc.11.2.18758