ArticleCancer science2019
IFN/STAT signaling controls tumorigenesis and the drug response in colorectal cancer.
Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 19 citations in OpenAlex.
- Ribosome biogenesis as a potential therapeutic target in KRAS mutant colorectal cancer.Nature communications · 2025Article
- Expression of Interleukin 23 and Interleukin 28 in Mucinous & Non-Mucinous Colorectal Carcinoma and Their Relation to Clinicopathological Features and Prognosis.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- A Case of APC Gene Mutation-Associated Familial Adenomatous Polyposis With Multiple System Malignancies.Cancer reports (Hoboken, N.J.) · 2025Article
- Nuclear adenomatous polyposis coli elevates STAT1 and reduces CXCL1,2, and 3 expression and inhibits neutrophil recruitment.Cellular signalling · 2025Article
- Unveiling the tumor microenvironment in colorectal cancer therapeutic resistance.Frontiers in cell and developmental biology · 2025Review
- Interplay between Signaling Pathways and Tumor Microenvironment Components: A Paradoxical Role in Colorectal Cancer.International journal of molecular sciences · 2023Review
- Long Non-coding RNA TPT1-AS1 Suppresses APC Transcription in a STAT1-Dependent Manner to Increase the Stemness of Colorectal Cancer Stem Cells.Molecular biotechnology · 2022Article
- A protocol for efficient CRISPR-Cas9-mediated knock-in in colorectal cancer patient-derived organoids.STAR protocols · 2021Article
- Proteasome inhibitors restore the STAT1 pathway and enhance the expression of MHC class I on human colon cancer cells.Journal of biomedical science · 2021Article
- Super-enhancer-associated long noncoding RNA RP11-569A11.1 inhibited cell progression and metastasis by regulating IFIT2 in colorectal cancer.Journal of clinical laboratory analysis · 2021Article
- Oncogenic KIT Modulates Type I IFN-Mediated Antitumor Immunity in GIST.Cancer immunology research · 2021Article
- Comparative Analysis of Patient-Matched PDOs Revealed a Reduction in OLFM4-Associated Clusters in Metastatic Lesions in Colorectal Cancer.Stem cell reports · 2021Article
- Regulation of signal transduction pathways in colorectal cancer: implications for therapeutic resistance.PeerJ · 2021Article
- Immune Microenvironment: New Insight for Familial Adenomatous Polyposis.Frontiers in oncology · 2021Review
- Evaluation of the RAS signaling network in response to MEK inhibition using organoids derived from a familial adenomatous polyposis patient.Scientific reports · 2020Article
- Organoid of ovarian cancer: genomic analysis and drug screening.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Review
- Nanoparticles Targeting STATs in Cancer Therapy.Cells · 2019Review
- IFN/STAT signaling controls tumorigenesis and the drug response in colorectal cancer.Cancer science · 2019Article
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
Abstract
Colorectal cancer (CRC) is caused by genetic alterations, and comprehensive sequence analyses have revealed the mutation landscapes. In addition to somatic changes, genetic variations are considered important factors contributing to tumor development; however, our knowledge on this subject is limited. Familial adenomatous polyposis coli (FAP) is an autosomal-dominant inherited disease caused by germline mutations in the adenomatous polyposis coli (APC) gene. FAP patients are classified into two major groups based on clinical manifestations: classical FAP (CFAP) and attenuated FAP (AFAP). In this study, we established 42 organoids from three CFAP patients and two AFAP patients. Comprehensive gene expression analysis demonstrated a close association between IFN/STAT signaling and the phenotypic features of FAP patients. Genetic disruption of Stat1 in the mouse model of FAP reduced tumor formation, demonstrating that the IFN/STAT pathway is causally associated with the tumor-forming potential of APC-deficient tumors. Mechanistically, STAT1 is downstream target of KRAS and is phosphorylated by its activating mutations. We found that enhanced IFN/STAT signaling in CFAP conferred resistance to MEK inhibitors. These findings reveal the crosstalk between RAS signaling and IFN/STAT signaling, which contributes to the tumor-forming potential and drug response. These results offer a rationale for targeting of IFN/STAT signaling and for the stratification of CRC patients.
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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.