ArticleNeoplasia (New York, N.Y.)2013
Ibuprofen inhibits colitis-induced overexpression of tumor-related Rac1b.
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. An erratum has been issued. Cited by 24 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.
The trial behind it
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
24 citing papers in PubMed, 36 citations in OpenAlex.
- Alternative Splicing at the Crossroad of Inflammatory Bowel Diseases and Colitis-Associated Colon Cancer.Cancers · 2025Review
- An integrated machine learning framework for developing and validating diagnostic models and drug predictions based on ulcerative colitis genes.Frontiers in medicine · 2025Article
- The Roles of RAC1 and RAC1B in Colorectal Cancer and Their Potential Contribution to Cetuximab Resistance.Cancers · 2024Review
- Novel 1,2,4-triazoles derived from Ibuprofen: synthesis and in vitro evaluation of their mPGES-1 inhibitory and antiproliferative activity.Molecular diversity · 2023Article
- Effects of Non-Opioid Analgesics on the Cell Membrane of Skin and Gastrointestinal Cancers.International journal of molecular sciences · 2022Review
- Pro-Inflammatory Cytokines Trigger the Overexpression of Tumour-Related Splice Variant RAC1B in Polarized Colorectal Cells.Cancers · 2022Article
- Ibuprofen disrupts a WNK1/GSK3β/SRPK1 protein complex required for expression of tumor-related splicing variant RAC1B in colorectal cells.Oncotarget · 2020Article
- The Small GTPase RAC1B: A Potent Negative Regulator of-and Useful Tool to Study-TGFβ Signaling.Cancers · 2020Review
- Review
- Splicing Busts a Move: Isoform Switching Regulates Migration.Trends in cell biology · 2020Review
- Inflammatory Microenvironment Modulation of Alternative Splicing in Cancer: A Way to Adapt.Advances in experimental medicine and biology · 2020Review
- Unveil the Anticancer Potential of Limomene Based Therapeutic Deep Eutectic Solvents.Scientific reports · 2019Article
- RAC1B: A Rho GTPase with Versatile Functions in Malignant Transformation and Tumor Progression.Cells · 2019Review
- Targeting the Eph/Ephrin System as Anti-Inflammatory Strategy in IBD.Frontiers in pharmacology · 2019Article
- The Rac1 splice form Rac1b favors mouse colonic mucosa regeneration and contributes to intestinal cancer progression.Oncogene · 2018Article
- Influence of transcriptional variants on metastasis.RNA biology · 2018Review
- Review
- The third dimension: new developments in cell culture models for colorectal research.Cellular and molecular life sciences : CMLS · 2016Review
- Article
- Tumor cell expression of MMP3 as a prognostic factor for poor survival in pancreatic, pulmonary, and mammary carcinoma.Genes & cancer · 2015Article
Corrections and comments
- Erratum issuedErratum to "Ibuprofen Inhibits Colitis-Induced Overexpression of Tumor-Related Rac1b" published in Neoplasia [15(1):102-111].2015 · Henriques, Andreia [Corrected to Henriques, Andreia F. A.]
Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The serrated pathway to colorectal tumor formation involves oncogenic mutations in the BRAF gene, which are sufficient for initiation of hyperplastic growth but not for tumor progression. A previous analysis of colorectal tumors revealed that overexpression of splice variant Rac1b occurs in around 80% of tumors with mutant BRAF and both events proved to cooperate in tumor cell survival. Here, we provide evidence for increased expression of Rac1b in patients with inflamed human colonic mucosa as well as following experimentally induced colitis in mice. The increase of Rac1b in the mouse model was specifically prevented by the nonsteroidal anti-inflammatory drug ibuprofen, which also inhibited Rac1b expression in cultured HT29 colorectal tumor cells through a cyclooxygenase inhibition.independent mechanism. Accordingly, the presence of ibuprofen led to a reduction of HT29 cell survival in vitro and inhibited Rac1b-dependent tumor growth of HT29 xenografts. Together, our results suggest that stromal cues, namely, inflammation, can trigger changes in Rac1b expression in the colon and identify ibuprofen as a highly specific and efficient inhibitor of Rac1b overexpression in colorectal tumors. Our data suggest that the use of ibuprofen may be beneficial in the treatment of patients with serrated colorectal tumors or with inflammatory colon syndromes.
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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.