ArticleOncoTargets and therapy2015
Polo-like kinase 2 acting as a promoter in human tumor cells with an abundance of TAp73.
Article in OncoTargets and therapy, 2015. 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, 17 citations in OpenAlex.
- Polo-Like Kinase 2: From Principle to Practice.Frontiers in oncology · 2022Review
- Circular RNA 0102049 suppresses the progression of osteosarcoma through modulating miR-520g-3p/PLK2 axis.Bioengineered · 2021Article
- Tumor suppressor PLK2 may serve as a biomarker in triple-negative breast cancer for improved response to PLK1 therapeutics.Cancer research communications · 2021Article
- Review
- Polo-like kinase 2 promotes chemoresistance and predicts limited survival benefit from adjuvant chemotherapy in colorectal cancer.International journal of oncology · 2018Article
- NVP-BEZ235 synergizes cisplatin sensitivity in osteosarcoma.Oncotarget · 2018Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTAp73, a member of the p53 tumor suppressor family, is frequently overexpressed in malignant tumors in humans. TAp73 abundance and phosphorylation modification result in variations in transcriptional activity. In a previous study, we found that the antitumor function of TAp73 was reactivated by dephosphorylation in head and neck squamous cell carcinomas. Polo-like kinase 2 (PLK2) displayed a close relationship with the p53 family in affecting the fate of cells. Herein, we investigate the hypothesis that PLK2 phosphorylates TAp73 and inhibits TAp73 function. MATERIALS AND
methodsHead and neck squamous cell carcinoma cell lines and osteosarcoma cell lines were used as natural models of the different expression levels of TAp73. Phosphorylation predictor software Scansite 3.0 and the predictor GPS-polo 1.0 were used to analyze the phosphorylation sites. Coimmunoprecipitation, phosphor-tag Western blot, metabolic labeling, and indirect immunofluorescence assays were used to determine the interactions between PLK2 and TAp73. TAp73 activity was assessed by Western blot and reverse transcription polymerase chain reaction, which we used to detect P21 and PUMA, both downstream genes of TAp73. The physiological effects of PLK2 cross talk with TAp73 on cell cycle progress and apoptosis were observed by flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling assays.
resultsPLK2 binds to and phosphorylates TAp73. PLK2 phosphorylates TAp73 at residue Ser48 and prohibits TAp73 translocation to the nucleus. Additionally, PLK2 inhibition combined with a DNA-damaging drug upregulated p21 and PUMA mRNA expression to a greater extent than DNA-damaging drug treatment alone. Inhibiting PLK2 in TAp73-enriched cells strengthened the effects of the DNA-damaging drug on both G1 phase arrest and apoptosis. Pretreatment with TAp73-siRNA weakened these effects.
conclusionThese findings reveal a novel PLK2 function (catalyzed phosphorylation of TAp73) which suppresses TAp73 functions. PLK2 promotes the survival of human tumor cells, a novel insight into the workings of malignant tumors characterized by TAp73 overexpression, and one that could speed the development of therapies.
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