ArticleOncotarget2016
p73 promotes glioblastoma cell invasion by directly activating POSTN (periostin) expression.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- A novel TAp73-inhibitory compound counteracts stemness features of glioblastoma stem cells.Molecular oncology · 2025Article
- Understanding glioblastoma stromal barriers against NK cell attack using tri-culture 3D spheroid model.Heliyon · 2024Article
- Identification of LOX as a candidate prognostic biomarker in Glioblastoma multiforme.Translational oncology · 2023Article
- DYRK1A-mediated PLK2 phosphorylation regulates the proliferation and invasion of glioblastoma cells.International journal of oncology · 2023Article
- Review
- Periostin: biology and function in cancer.Cancer cell international · 2022Review
- Differences in the Expression Patterns ofCancers · 2022Article
- Review
- The p53 family member p73 in the regulation of cell stress response.Biology direct · 2021Review
- Article
- Quail-chick grafting experiments corroborate that Tbr1-positive eminential prethalamic neurons migrate along three streams into hypothalamus, subpallium and septocommissural areas.Brain structure & function · 2021Article
- p73 as a Tissue Architect.Frontiers in cell and developmental biology · 2021Review
- Combined treatment with CBP and BET inhibitors reverses inadvertent activation of detrimental super enhancer programs in DIPG cells.Cell death & disease · 2020Article
- p53-Related Transcription Targets of TAp73 in Cancer Cells-Bona Fide or Distorted Reality?International journal of molecular sciences · 2020Review
- Integrated transcriptomic analysis reveals hub genes involved in diagnosis and prognosis of pancreatic cancer.Molecular medicine (Cambridge, Mass.) · 2019Article
- Zika virus infection induces MiR34c expression in glioblastoma stem cells: new perspectives for brain tumor treatments.Cell death & disease · 2019Article
- The lncRNA TP73-AS1 is linked to aggressiveness in glioblastoma and promotes temozolomide resistance in glioblastoma cancer stem cells.Cell death & disease · 2019Article
- Clinical implications of the deregulated TP73 isoforms expression in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018Review
- Periostin silencing suppresses the aggressive phenotype of thyroid carcinoma cells by suppressing the Akt/thyroid stimulating hormone receptor axis.Cytotechnology · 2018Article
- Cross-species transcriptional analysis reveals conserved and host-specific neoplastic processes in mammalian glioma.Scientific reports · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Glioblastoma Multiforme is one of the most highly metastatic cancers and constitutes 70% of all gliomas. Despite aggressive treatments these tumours have an exceptionally bad prognosis, mainly due to therapy resistance and tumour recurrence. Here we show that the transcription factor p73 confers an invasive phenotype by directly activating expression of POSTN (periostin, HGNC:16953) in glioblastoma cells. Knock down of endogenous p73 reduces invasiveness and chemo-resistance, and promotes differentiation in vitro. Using chromatin immunoprecipitation and reporter assays we demonstrate that POSTN, an integrin binding protein that has recently been shown to play a major role in metastasis, is a transcriptional target of TAp73. We further show that POSTN overexpression is sufficient to rescue the invasive phenotype of glioblastoma cells after p73 knock down. Additionally, bioinformatics analysis revealed that an intact p73/ POSTN axis, where POSTN and p73 expression is correlated, predicts bad prognosis in several cancer types. Taken together, our results support a novel role of TAp73 in controlling glioblastoma cell invasion by regulating the expression of the matricellular protein POSTN.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.