ArticleThe Journal of biological chemistry2010
Overexpression of the pituitary tumor transforming gene induces p53-dependent senescence through activating DNA damage response pathway in normal human fibroblasts.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Comparative Meta-Analysis of Transcriptomics Data during Cellular Senescence and In Vivo Tissue Ageing.Oxidative medicine and cellular longevity · 2015Pooled it
- Early life exposure to N-nitrosamine drives genotoxicity, mutagenesis, and tumorigenesis in DNA repair-deficient mice.Nature communications · 2026Article
- Postbiotics Combination Synergises the Antiproliferative Effects of Doxorubicin in Gastric Cancer Cells: A Cellular and Molecular Deep Dive.International journal of molecular sciences · 2025Article
- RNA sequencing identifiesCytotechnology · 2025Article
- Cell senescence-associated genes predict the malignant characteristics of glioblastoma.Cancer cell international · 2022Article
- Article
- Alteration of Pituitary Tumor Transforming Gene 1 by MicroRNA-186 and 655 Regulates Invasion Ability of Human Oral Squamous Cell Carcinoma.International journal of molecular sciences · 2021Article
- Falcarindiol Enhances Cisplatin Chemosensitivity of Hepatocellular CarcinomaFrontiers in pharmacology · 2021Article
- Of mice, genes and aging.Haematologica · 2020Article
- Article
- The lifespan quantitative trait locus geneHaematologica · 2020Article
- PTTG and PBF Functionally Interact with p53 and Predict Overall Survival in Head and Neck Cancer.Cancer research · 2018Article
- Synthetic lethal genetic interactions between Rad54 and PARP-1 in mouse development and oncogenesis.Oncotarget · 2017Article
- Elevated PTTG and PBF predicts poor patient outcome and modulates DNA damage response genes in thyroid cancer.Oncogene · 2017Article
- Conserved genes and pathways in primary human fibroblast strains undergoing replicative and radiation induced senescence.Biological research · 2016Article
- Development of a Bifunctional Andrographolide-Based Chemical Probe for Pharmacological Study.PloS one · 2016Article
- Alteration of Pituitary Tumor Transforming Gene-1 Regulates Trophoblast Invasion via the Integrin/Rho-Family Signaling Pathway.PloS one · 2016Article
- High expression of pituitary tumor-transforming gene-1 predicts poor prognosis in clear cell renal cell carcinoma.Molecular and clinical oncology · 2015Article
- Pituitary tumor-transforming gene 1 (PTTG1) is overexpressed in oral squamous cell carcinoma (OSCC) and promotes migration, invasion and epithelial-mesenchymal transition (EMT) in SCC15 cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Radiation induces senescence and a bystander effect through metabolic alterations.Cell death & disease · 2014Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pituitary tumor transforming gene (PTTG1, securin) is involved in cell-cycle control through inhibition of sister-chromatid separation. Elevated levels of PTTG1 were found to be associated with many different tumor types that might be involved in late stage tumor progression. However, the role of PTTG1 in early stage of tumorigenesis is unclear. Here we utilized the adenovirus expression system to deliver PTTG1 into normal human fibroblasts to evaluate the role of PTTG1 in tumorigenesis. Expressing PTTG1 in normal human fibroblasts inhibited cell proliferation. Several senescence-associated (SA) phenotypes including increased SA-beta-galactosidase activities, decreased bromodeoxyuridine incorporation, and increased SA-heterochromatin foci formation were also observed in PTTG1-expressing cells, indicating that PTTG1 overexpression induced a senescent phenotype in normal cells. Significantly, the PTTG1-induced senescence is p53-dependent and telomerase-independent, which is distinctively different from that of replicative senescence. The mechanism of PTTG1-induced senescence was also analyzed. Consistent with its role in regulating sister-chromatid separation, overexpression of PTTG1 inhibited the activation of separase. Consequently, the numbers of cells with abnormal nuclei morphologies and chromosome separations were increased, which resulted in activation of the DNA damage response. Thus, we concluded that PTTG1 overexpression in normal human fibroblasts caused chromosome instability, which subsequently induced p53-dependent senescence through activation of DNA-damage response pathway.
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