ArticleOncogene2009
Plk1 regulates liver tumor cell death by phosphorylation of TAp63.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 35 citations in OpenAlex.
- Regulation of doxorubicin resistance and cellular metabolism by miR-203a-3p via p53 and TAp63 signaling in hepatocellular carcinoma.Frontiers in pharmacology · 2026Article
- DENetwork unveils non-differentially expressed genes with functional relevance across conditions through information flow perturbation.Nucleic acids research · 2025Article
- Kelch-like proteins in the gastrointestinal tumors.Acta pharmacologica Sinica · 2023Review
- Single-cell transcriptomics reveals the role of Macrophage-Naïve CD4 + T cell interaction in the immunosuppressive microenvironment of primary liver carcinoma.Journal of translational medicine · 2022Article
- Article
- The Regulation of Tumor Suppressor p63 by the Ubiquitin-Proteasome System.International journal of molecular sciences · 2016Review
- Combined Inhibition of MEK and Plk1 Has Synergistic Antitumor Activity in NRAS Mutant Melanoma.The Journal of investigative dermatology · 2015Article
- Receptor-type protein tyrosine phosphatase κ directly dephosphorylates CD133 and regulates downstream AKT activation.Oncogene · 2015Article
- Regulation of p63 protein stability via ubiquitin-proteasome pathway.BioMed research international · 2014Review
- The role of polo-like kinase 1 in carcinogenesis: cause or consequence?Cancer research · 2013Review
- Pro-apoptotic TP53 homolog TAp63 is repressed via epigenetic silencing and B-cell receptor signalling in chronic lymphocytic leukaemia.British journal of haematology · 2013Article
- 15-hydroxyprostaglandin dehydrogenase-derived 15-keto-prostaglandin E2 inhibits cholangiocarcinoma cell growth through interaction with peroxisome proliferator-activated receptor-γ, SMAD2/3, and TAP63 proteins.The Journal of biological chemistry · 2013Article
- Battle of the eternal rivals: restoring functional p53 and inhibiting Polo-like kinase 1 as cancer therapy.Oncotarget · 2013Review
- Phosphorylation of ΔNp63α via a novel TGFβ/ALK5 signaling mechanism mediates the anti-clonogenic effects of TGFβ.PloS one · 2012Article
- p53: the attractive tumor suppressor in the cancer research field.Journal of biomedicine & biotechnology · 2011Review
- p73-Binding Partners and Their Functional Significance.International journal of proteomics · 2010Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously found that Plk1 inhibited the p53/p73 activity through its direct phosphorylation. In this study, we investigated the functional role of Plk1 in modulating the p53 family member TAp63, resulting in the control of apoptotic cell death in liver tumor cells. Immunoprecipitation and in vitro pull-down assay showed that p63 binds to the kinase domain of Plk1 through its DNA-binding region. in vitro kinase assay indicated that p63 is phosphorylated by Plk1 at Ser-52 of the transactivating (TA) domain. Plk1 decreased the protein stability of TAp63 by its phosphorylation and suppressed TAp63-induced cell death. Furthermore, Plk1 knockdown in p53-mutated liver tumor cells transactivated p53 family downstream effectors, PUMA, p21(Cip1/WAF1) and 14-3-3sigma, and induced apoptotic cell death. Double knockdown of Plk1/p63 attenuated Plk1 knockdown-induced apoptotic cell death and transactivation. Intriguingly, both Plk1 and p63 are highly expressed in the side population (SP) fraction of liver tumor cells compared to non-SP fraction cells, suggesting the significance of Plk1/TAp63 in the control of cell death in tumor-initiating SP fraction cells. Thus, Plk1 controls TAp63 by its phosphorylation and regulates apoptotic cell death in liver tumor cells. Plk1/TAp63 may be a suitable candidate as a molecular target of liver tumor treatments.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.