ArticleNeoplasia (New York, N.Y.)2013
Interleukin-1β promotes ovarian tumorigenesis through a p53/NF-κB-mediated inflammatory response in stromal fibroblasts.
Article in Neoplasia (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 89 citations in OpenAlex.
- Cytokines and cancer-associated fibroblasts.Journal of hematology & oncology · 2026Review
- TAK1 inhibition restores p53 expression and suppresses inflammation and hyperplasia in JIA synovial fibroblasts.Rheumatology (Oxford, England) · 2026Article
- Prognostic Significance and Emerging Predictive Potential of Interleukin-1β Expression in Oncogene-Driven NSCLC.Cancers · 2025Article
- Crosstalk between cancer‑associated fibroblasts and inflammation in tumor microenvironment: A novel perspective in cancer therapy (Review).Oncology reports · 2025Review
- Nervonic acid triggered ovarian inflammation by inducing mitochondrial oxidative stress to activate NLRP3/ IL-1β pathway.Journal of advanced research · 2025Article
- Interleukin-1β Inhibits Ovarian Cancer Cell Proliferation and Metastasis Through the MAPK/MMP12 Pathway.International journal of molecular sciences · 2025Article
- The role of transcription factors in the crosstalk between cancer-associated fibroblasts and tumor cells.Journal of advanced research · 2025Review
- Interleukin-6 Modulation in Ovarian Cancer Necessitates a Targeted Strategy: From the Approved to Emerging Therapies.Cancers · 2024Review
- Bioinformatic and experimental data pertaining to the role of the NLRP3 inflammasome in ovarian cancer.Journal of cancer research and clinical oncology · 2024Review
- p53 at the crossroads of tumor immunity.Nature cancer · 2024Review
- Sol-gel synthesis and cytotoxicity evaluation of selenium-doped cerium oxide nanoparticles for biomedical applications.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Crosstalk between cancer-associated fibroblasts and regulated cell death in tumors: insights into apoptosis, autophagy, ferroptosis, and pyroptosis.Cell death discovery · 2024Review
- Ovarian tumor microenvironment contributes to tumor progression and chemoresistance.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Combined dandelion extract and all-trans retinoic acid induces cytotoxicity in human breast cancer cells.Scientific reports · 2023Article
- Prevention of Epithelial Ovarian Cancer.Cold Spring Harbor perspectives in medicine · 2023Review
- Autophagy in Cancer Immunotherapy.Cells · 2022Review
- Deciphering the immune landscape dominated by cancer-associated fibroblasts to investigate their potential in indicating prognosis and guiding therapeutic regimens in high grade serous ovarian carcinoma.Frontiers in immunology · 2022Article
- Immunological configuration of ovarian carcinoma: features and impact on disease outcome.Journal for immunotherapy of cancer · 2021Review
- Review
- N-acetyl cysteine induces quiescent-like pancreatic stellate cells from an active state and attenuates cancer-stroma interactions.Journal of experimental & clinical cancer research : CR · 2021Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Cancer has long been considered a disease that mimics an "unhealed wound," with oncogene-induced secretory activation signals from epithelial cancer cells facilitating stromal fibroblast, endothelial, and inflammatory cell participation in tumor progression. However, the underlying mechanisms that orchestrate cooperative interaction between malignant epithelium and the stroma remain largely unknown. Here, we identified interleukin-1β (IL-1β) as a stromal-acting chemokine secreted by ovarian cancer cells, which suppresses p53 protein expression in cancer-associated fibroblasts (CAFs). Elevated expression of IL-1β and cognate receptor IL-1R1 in ovarian cancer epithelial cells and CAFs independently predicted reduced overall patient survival, as did repressed nuclear p53 in ovarian CAFs. Knockdown of p53 expression in ovarian fibroblasts significantly enhanced the expression and secretion of chemokines IL-8, growth regulated oncogene-alpha (GRO-α), IL-6, IL-1β, and vascular endothelial growth factor (VEGF), significantly increased in vivo mouse xenograft ovarian cancer tumor growth, and was entirely dependent on interaction with, and transcriptional up-regulation of, nuclear factor-kappaB (NF-κB) p65. Our results have uncovered a previously unrecognized circuit whereby epithelial cancer cells use IL-1β as a communication factor instructing stromal fibroblasts through p53 to generate a protumorigenic inflammatory microenvironment. Attenuation of p53 protein expression in stromal fibroblasts generates critical protumorigenic functionality, reminiscent of the role that oncogenic p53 mutations play in cancer cells. These findings implicate CAFs as an important target for blocking inflammation in the tumor microenvironment and reducing tumor growth.
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