ArticleGenes & development2016
Opposing effects of TIGAR- and RAC1-derived ROS on Wnt-driven proliferation in the mouse intestine.
Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 106 citations in OpenAlex.
- The lipid transfer protein STARD7 controls intestinal tumor development in a context-dependent manner.EMBO molecular medicine · 2026Article
- Cancer-specific Regulation of Metabolic and Epigenetic Pathways by Dietary Phytochemicals.Pharmaceutical research · 2025Review
- The Role of Reactive Oxygen Species in Colorectal Cancer Initiation and Progression: Perspectives on Theranostic Approaches.Cancers · 2025Review
- Reactive Oxygen Species and its Manipulation Strategies in Cancer Treatment.Current medicinal chemistry · 2025Review
- Eosinophils in inflammatory bowel disease pathogenesis: an ROS-centric view.Frontiers in allergy · 2025Article
- In vivo Therapeutic Inhibition of the Tp53-Induced Glycolysis and Apoptosis Regulator (TIGAR) by Intravenous Administration of an Anti-Oncological siRNA-Biopolymer, TI6752 (Tituxistatin), in a Preclinical Xenograft Model of Colorectal Cancer.Journal of experimental pharmacology · 2025Article
- Regulation of ROS signaling by TIGAR induces cancer-modulating responses in the tumor microenvironment.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- WDR12/RAC1 axis promoted proliferation and anti-apoptosis in colorectal cancer cells.Molecular and cellular biochemistry · 2024Article
- The potential of aryl hydrocarbon receptor as receptors for metabolic changes in tumors.Frontiers in oncology · 2024Review
- Tigecycline causes loss of cell viability mediated by mitochondrial OXPHOS and RAC1 in hepatocellular carcinoma cells.Journal of translational medicine · 2023Article
- Multifaceted role of redox pattern in the tumor immune microenvironment regarding autophagy and apoptosis.Molecular cancer · 2023Review
- Article
- Metabolism and Colorectal Cancer.Annual review of pathology · 2023Review
- NADPH-dependent ROS accumulation contributes to the impaired osteogenic differentiation of periodontal ligament stem cells under high glucose conditions.Frontiers in endocrinology · 2023Article
- Harnessing Redox Disruption to Treat Human Herpesvirus 8 (HHV-8) Related Malignancies.Antioxidants (Basel, Switzerland) · 2022Review
- Extrinsic cell death pathway plasticity: a driver of clonal evolution in cancer?Cell death discovery · 2022Review
- Non-enzymatic role of SOD1 in intestinal stem cell growth.Cell death & disease · 2022Article
- Increased mtDNA mutation frequency in oocytes causes epigenetic alterations and embryonic defects.National science review · 2022Article
- The role of ROS in tumour development and progression.Nature reviews. Cancer · 2022Review
- The role of TIGAR in nervous system diseases.Frontiers in aging neuroscience · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) participate in numerous cell responses, including proliferation, DNA damage, and cell death. Based on these disparate activities, both promotion and inhibition of ROS have been proposed for cancer therapy. However, how the ROS response is determined is not clear. We examined the activities of ROS in a model of Apc deletion, where loss of the Wnt target gene Myc both rescues APC loss and prevents ROS accumulation. Following APC loss, Myc has been shown to up-regulate RAC1 to promote proliferative ROS through NADPH oxidase (NOX). However, APC loss also increased the expression of TIGAR, which functions to limit ROS. To explore this paradox, we used three-dimensional (3D) cultures and in vivo models to show that deletion of TIGAR increased ROS damage and inhibited proliferation. These responses were suppressed by limiting damaging ROS but enhanced by lowering proproliferative NOX-derived ROS. Despite having opposing effects on ROS levels, loss of TIGAR and RAC1 cooperated to suppress intestinal proliferation following APC loss. Our results indicate that the pro- and anti-proliferative effects of ROS can be independently modulated in the same cell, with two key targets in the Wnt pathway functioning to integrate the different ROS signals for optimal cell proliferation.
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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.