ReviewBreast cancer research : BCR2013
Tissue transglutaminase as a central mediator in inflammation-induced progression of breast cancer.
Review in Breast cancer research : BCR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
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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
62 citing papers in PubMed, 99 citations in OpenAlex.
- Oxaliplatin-induced testicular toxicity is associated with transglutaminase-4 upregulation, hormonal dysregulation, and inflammatory responses.Journal of applied biomedicine · 2026Article
- Review
- Removal or inhibition of transglutaminase 2 decreases cellular stress, supporting tissue preservation, and recovery after SCI.Acta neuropathologica communications · 2025Article
- TGM2 regulated by transcription factor NR3C1 drives p38 MAPK-mediated tumor progression and immune evasion in lung squamous cell carcinoma.Frontiers in immunology · 2025Article
- Article
- Transglutaminase 2-mediated histone monoaminylation and its role in cancer.Bioscience reports · 2024Review
- Bioorthogonal Labeling and Enrichment of Histone Monoaminylation Reveal Its Accumulation and Regulatory Function in Cancer Cell Chromatin.Journal of the American Chemical Society · 2024Article
- The upregulation of TGM2 is associated with poor prognosis and the shaping of the inflammatory tumor microenvironment in lung squamous cell carcinoma.American journal of cancer research · 2024Article
- Transglutaminase 2 in breast cancer metastasis and drug resistance.Frontiers in cell and developmental biology · 2024Review
- An immunogenic cell death-related signature predicts prognosis and immunotherapy response in stomach adenocarcinoma.Apoptosis : an international journal on programmed cell death · 2023Article
- TheFoods (Basel, Switzerland) · 2023Article
- High and Low Levels ofInternational journal of molecular sciences · 2023Article
- The Role ofInternational journal of molecular sciences · 2023Article
- A bioinformatics analysis and an experimental validation of the hypoxia-related prognostic model.Journal of gastrointestinal oncology · 2023Article
- SDC1-TGM2-FLOT1-BHMT complex determines radiosensitivity of glioblastoma by influencing the fusion of autophagosomes with lysosomes.Theranostics · 2023Article
- TG2 as a novel breast cancer prognostic marker promotes cell proliferation and glycolysis by activating the MEK/ERK/LDH pathway.BMC cancer · 2022Article
- Faecal Proteomics and Functional Analysis of Equine Melanocytic Neoplasm in Grey Horses.Veterinary sciences · 2022Article
- Dysregulation of Transglutaminase type 2 through GATA3 defines aggressiveness and Doxorubicin sensitivity in breast cancer.International journal of biological sciences · 2022Article
- Interleukin-32 regulates downstream molecules and promotes the invasion of pancreatic cancer cells.Oncology letters · 2022Article
- NF-κB Signaling in Tumor Pathways Focusing on Breast and Ovarian Cancer.Oncology reviews · 2022Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
TGM2 is a stress-responsive gene that encodes a multifunctional and structurally complex protein called tissue transglutaminase (abbreviated as TG2 or tTG). TGM2 expression is frequently upregulated during inflammation and wounding. Emerging evidence indicates that TGM2 expression is aberrantly upregulated in multiple cancer cell types, particularly those selected for resistance to chemotherapy and radiation therapy and those isolated from metastatic sites. It is becoming increasingly evident that chronic expression of TG2 in epithelial cancer cells initiates a complex series of signaling networks which contributes to the development of drug resistance and an invasive phenotype. For example, forced or basal high expression of TG2 in mammary epithelial cells is associated with activation of nuclear transcription factor-kappa B (NF-κB), Akt, focal adhesion kinase, and hypoxia-inducible factor. All of these changes are considered hallmarks of aggressive tumors. TG2 expression is able to induce the developmentally regulated program of epithelial-to-mesenchymal transition (EMT) and to confer cancer stem cell (CSC) traits in mammary epithelial cells; both EMT and CSCs have been implicated in cancer metastasis and resistance to standard therapies. Importantly, TG2 expression in tumor samples is associated with poor disease outcome, increased drug resistance, and increased incidence of metastasis. These observations imply that TG2 plays a crucial role in promoting an aggressive phenotype in mammary epithelial cells. In this review, we discuss recent evidence that TG2-regulated pathways contribute to the aggressive phenotype in breast cancer.
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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 OpenQuestion graph.