ArticleOncotarget2015
p53 amplifies Toll-like receptor 5 response in human primary and cancer cells through interaction with multiple signal transduction pathways.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- p53-responsive TLR8 SNP enhances human innate immune response to respiratory syncytial virus.The Journal of clinical investigation · 2019Trial
- TP53 Loss Elevates NF-κB-IFN-β-MHC-Ia Signaling to Promote NK Cell Resistance in Osteosarcoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Toll-Like Receptors in the Immunotherapy Era: Dual-Edged Swords of Tumor Immunity and Clinical Translation.MedComm · 2025Review
- Mechanistic Exploration ofPharmaceuticals (Basel, Switzerland) · 2024Article
- p53 at the crossroads of tumor immunity.Nature cancer · 2024Review
- Combining p53 mRNA nanotherapy with immune checkpoint blockade reprograms the immune microenvironment for effective cancer therapy.Nature communications · 2022Article
- p53 signaling in cancer progression and therapy.Cancer cell international · 2021Review
- Dietary Flavonoids in p53-Mediated Immune Dysfunctions Linking to Cancer Prevention.Biomedicines · 2020Review
- Mutant p53 as an Antigen in Cancer Immunotherapy.International journal of molecular sciences · 2020Review
- P53: A Guardian of Immunity Becomes Its Saboteur through Mutation.International journal of molecular sciences · 2020Review
- Polygonatum sibiricum polysaccharide potentially attenuates diabetic retinal injury in a diabetic rat model.Journal of diabetes investigation · 2019Article
- Are lung adenocarcinoma mutations shaping the immune microenvironment?Translational cancer research · 2018Article
- The Cytidine Deaminase APOBEC3 Family Is Subject to Transcriptional Regulation by p53.Molecular cancer research : MCR · 2017Article
- Nuclear localization of Toll-like receptor 5 in Barrett's esophagus and esophageal adenocarcinoma is associated with metastatic behavior.Virchows Archiv : an international journal of pathology · 2016Article
- Ligand dependent restoration of human TLR3 signaling and death in p53 mutant cells.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The p53 tumor suppressor regulates transcription of genes associated with diverse cellular functions including apoptosis, growth arrest, DNA repair and differentiation. Recently, we established that p53 can modulate expression of Toll-like receptor (TLR) innate immunity genes but the degree of cross-talk between p53 and TLR pathways remained unclear. Here, using gene expression profiling we characterize the global effect of p53 on the TLR5-mediated transcription in MCF7 cells. We found that combined activation of p53 and TLR5 pathways synergistically increases expression of over 200 genes, mostly associated with immunity and inflammation. The synergy was observed in several human cancer cells and primary lymphocytes. The p53-dependent amplification of transcriptional response to TLR5 activation required expression of NFκB subunit p65 and was mediated by several molecular mechanisms including increased phosphorylation of p38 MAP kinase, PI3K and STAT3 signaling. Additionally, p53 induction increased cytokine expression in response to TNFα, another activator of NFκB and MAP kinase pathways, suggesting a broad interaction between p53 and these signaling pathways. The expression of many synergistically induced genes is elevated in breast cancer patients responsive to chemotherapy. We suggest that p53's capacity to enhance immune response could be exploited to increase antitumor immunity and to improve cancer treatment.
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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.