ArticleFrontiers in oncology2014
The Role of STAT1 for Crosstalk between Fibroblasts and Colon Cancer Cells.
Article in Frontiers in oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Advancements in 3D In Vitro Models for Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Fibroblasts as Turned Agents in Cancer Progression.Cancers · 2023Review
- A chemical probe inhibitor targeting STAT1 restricts cancer stem cell traits and angiogenesis in colorectal cancer.Journal of biomedical science · 2022Article
- Anti-Cancer Pectins and Their Role in Colorectal Cancer Treatment.Onco therapeutics · 2022Article
- USP22 deficiency in melanoma mediates resistance to T cells through IFNγ-JAK1-STAT1 signal axis.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Acquired radioresistance in cancer associated fibroblasts is concomitant with enhanced antioxidant potential and DNA repair capacity.Cell communication and signaling : CCS · 2021Article
- Angiogenin regulates PKD activation and COX-2 expression induced by TNF-α and bradykinin in the colonic myofibroblast.Biochemical and biophysical research communications · 2020Article
- Investigation of health benefits of cocoa in human colorectal cancer cell line, HT-29 through interactome analysis.Gastroenterology and hepatology from bed to bench · 2019Article
- Impact of Cancer-Associated Fibroblast on the Radiation-Response of Solid Xenograft Tumors.Frontiers in molecular biosciences · 2019Article
- Deficiency in STAT1 Signaling Predisposes Gut Inflammation and Prompts Colorectal Cancer Development.Cancers · 2018Article
- Pectin Oligosaccharides Ameliorate Colon Cancer by Regulating Oxidative Stress- and Inflammation-Activated Signaling Pathways.Frontiers in immunology · 2018Review
- Targeting Oncogenic Transcription Factors: Therapeutic Implications of Endogenous STAT Inhibitors.Trends in cancer · 2017Review
- Proteins are potent biomarkers to detect colon cancer progression.Saudi journal of biological sciences · 2017Article
- The ratio of STAT1 to STAT3 expression is a determinant of colorectal cancer growth.Oncotarget · 2016Article
- Integrating Immunologic Signaling Networks: The JAK/STAT Pathway in Colitis and Colitis-Associated Cancer.Vaccines · 2016Review
- Nanoparticle modulation of the tumor microenvironment enhances therapeutic efficacy of cisplatin.Journal of controlled release : official journal of the Controlled Release Society · 2015Article
- Supportive and rejective functions of tumor stroma on tumor cell growth, survival, and invasivity: the cancer evolution.Frontiers in oncology · 2015Article
- Prognostic and Predictive Significance of Stromal Fibroblasts and Macrophages in Colon Cancer.Biomarkers in cancer · 2015Review
- Cancer-associated fibroblasts connect metastasis-promoting communication in colorectal cancer.Frontiers in oncology · 2015Review
- A pan-cancer modular regulatory network analysis to identify common and cancer-specific network components.Cancer informatics · 2014Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signaling between tumor cells and the associated stroma has an important impact on cancer initiation and progression. The tumor microenvironment has a paradoxical role in tumor progression and fibroblasts, a major component of the tumor stroma, have been shown to either inhibit or promote cancer development. In this study, we established that normal intestinal fibroblasts activate STAT1 signaling in colon cancer cells and, in contrast to cancer-associated fibroblasts, inhibit growth of tumor cells. Treatment of 18Co fibroblasts with the proinflammatory cytokine TNFα interfered with their ability to trigger STAT1 signaling in cancer cells. Accordingly, intestinal myofibroblasts isolated from patients with ulcerative colitis or Crohn's disease, which are activated and produce high levels of TNFα, failed to stimulate STAT1 signaling in tumor cells, demonstrating that activated myofibroblasts lose the ability to trigger growth-inhibitory STAT1 signaling in tumor cells. Finally, we confirmed that silencing of STAT1 in tumor cells alters the crosstalk between tumor cells and fibroblasts, suggesting STAT1 as a novel link between intestinal inflammation and colon cancer. We demonstrated that normal fibroblasts restrain the growth of carcinoma cells, at least in part, through the induction of STAT1 signaling in cancer cells and showed that changes in the microenvironment, as they occur in inflammatory bowel disease, alter the crosstalk between carcinoma cells and fibroblasts, perturb the homeostasis of intestinal tissue, and thereby contribute to tumor progression.
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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.