ArticleAmerican journal of cancer research2014
STAT3β controls inflammatory responses and early tumor onset in skin and colon experimental cancer models.
Article in American journal of cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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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
16 citing papers in PubMed, 23 citations in OpenAlex.
- Colitis-Associated Colorectal Cancer-STAT3 Inhibition as a Preventive Strategy.International journal of molecular sciences · 2026Article
- STAT3 Inhibition to Treat Ulcerative Colitis-Associated Colorectal Cancer.International journal of molecular sciences · 2025Article
- Probing the Depths of Molecular Complexity: STAT3 as a Key Architect in Colorectal Cancer Pathogenesis.Current gene therapy · 2025Review
- Therapeutic Potential of a Small-Molecule STAT3 Inhibitor in a Mouse Model of Colitis.Cancers · 2023Article
- Article
- Targeting key transcriptional factor STAT3 in colorectal cancer.Molecular and cellular biochemistry · 2021Review
- Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 to Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution.Pharmacological reviews · 2020Review
- A deep intronic splice mutation ofProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Targeted inhibition of STAT3 as a potential treatment strategy for atherosclerosis.Theranostics · 2019Review
- PCBP1 inhibits the expression of oncogenic STAT3 isoform by targeting alternative splicing of STAT3 exon 23.International journal of biological sciences · 2019Article
- Synbiotics suppress colitis-induced tumorigenesis in a colon-specific cancer mouse model.PloS one · 2019Article
- The Highly Pure Neem Leaf Extract, SCNE, Inhibits Tumorigenesis in Oral Squamous Cell Carcinoma via Disruption of Pro-tumor Inflammatory Cytokines and Cell Signaling.Frontiers in oncology · 2019Article
- Nucleus, Mitochondrion, or Reticulum? STAT3 à La Carte.International journal of molecular sciences · 2018Review
- Reg3g Promotes Pancreatic Carcinogenesis in a Murine Model of Chronic Pancreatitis.Digestive diseases and sciences · 2015Article
- Emerging translational approaches to target STAT3 signalling and its impact on vascular disease.Cardiovascular research · 2015Review
- Curcumin suppresses invasiveness and vasculogenic mimicry of squamous cell carcinoma of the larynx through the inhibition of JAK-2/STAT-3 signaling pathway.American journal of cancer research · 2015Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 4 countries.
Funding
Abstract
Chronic inflammation is a well-recognized pathogenic factor in tumor initiation and progression. Mice lacking the pro-oncogenic transcription factor STAT3 were shown to be protected from both colitis-associated and epidermal cancers induced by the AOM/DSS and DMBA/TPA protocols, respectively. However, these murine models did not distinguish between the two STAT3 isoforms, the full-length STAT3α, believed to exert most pro-oncogenic functions attributed to STAT3, and the shorter STAT3β, often referred to as a dominant-negative, but possessing specific transcriptional activities. Here we assessed the contribution of STAT3β to inflammation-driven tumorigenesis making use of mice lacking this isoform, but still expressing STAT3α (STAT3(Δβ/Δβ)). We show that the lack of STAT3β leads to exacerbated acute responses to both TPA and DSS, thus confirming its anti-inflammatory role. Enhanced inflammation correlates with earlier tumor onset in both the epidermis and the intestine in STAT3(Δβ/Δβ) mice. In contrast, overall tumor development and final tumor burden were unaffected. These results suggest that STAT3β, by limiting inflammation during the initial phases of tumorigenesis, contributes to tissue homeostasis and counteracts malignant transformation and initial tumor growth. Accordingly, the balance between the two STAT3 isoforms, likely determined by the complex signaling networks shaping the tumor microenvironment and driving tumor transformation and progression, is apparently crucial to determine the initial tumor transformation rates in inflammation-associated cancers.
Indexed as
Identifiers
25232490PMC4163613W1764343818What OpenQuestion 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 OpenQuestion graph.