ArticleNature communications2017
Contribution of classical end-joining to PTEN inactivation in p53-mediated glioblastoma formation and drug-resistant survival.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
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- Targeting CK2 in cancer: a valuable strategy or a waste of time?Cell death discovery · 2021Review
- CXCL12 enhances pregnancy outcome via improvement of endometrial receptivity in mice.Scientific reports · 2021Article
- Profilin-1; a novel regulator of DNA damage response and repair machinery in keratinocytes.Molecular biology reports · 2021Article
- Significant value of XRCC2 and XRCC9 expression in the prognosis of human ovarian carcinoma.Journal of Cancer · 2021Article
- Eupatilin treatment inhibits transforming growth factor beta-induced endometrial fibrosis in vitro.Clinical and experimental reproductive medicine · 2020Article
- Endometrial profilin 1: a key player in embryo-endometrial crosstalk.Clinical and experimental reproductive medicine · 2020Article
- Role of Asparagine Endopeptidase in Mediating Wild-Type p53 Inactivation of Glioblastoma.Journal of the National Cancer Institute · 2020Article
- Role of protein kinase CK2 in antitumor drug resistance.Journal of experimental & clinical cancer research : CR · 2019Review
- Involvement of Phosphatase and Tensin Homolog in Cyclin-Dependent Kinase 4/6 Inhibitor-Induced Blockade of Glioblastoma.Frontiers in pharmacology · 2019Article
- Enhanced breast cancer progression by mutant p53 is inhibited by the circular RNA circ-Ccnb1.Cell death and differentiation · 2018Article
- A protocol for custom CRISPR Cas9 donor vector construction to truncate genes in mammalian cells using pcDNA3 backbone.BMC molecular biology · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
DNA repair gene defects are found in virtually all human glioblastomas, but the genetic evidence for a direct role remains lacking. Here we demonstrate that combined inactivation of the XRCC4 non-homologous end-joining (NHEJ) DNA repair gene and p53 efficiently induces brain tumours with hallmark characteristics of human proneural/classical glioblastoma. The murine tumours exhibit PTEN loss of function instigated by reduced PTEN mRNA, and increased phosphorylated inactivation and stability as a consequence of aberrantly elevated CK2 provoked by p53 ablation and irrevocably deregulated by NHEJ inactivation. This results in DNA damage-resistant cytoplasmic PTEN and CK2 expression, and the attenuation of DNA repair genes. CK2 inhibition restores PTEN nuclear distribution and DNA repair activities and impairs tumour but not normal cell survival. These observations demonstrate that NHEJ contributes to p53-mediated glioblastoma suppression, and reveal a crucial role for PTEN in the early DNA damage signalling cascade, the inhibition of which promotes tumorigenicity and drug-resistant survival.
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