ArticleGastroenterology2021
DDIT4 Licenses Only Healthy Cells to Proliferate During Injury-induced Metaplasia.
Article in Gastroenterology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
- Global research trends in signaling pathways of spasmolytic polypeptide-expressing metaplasia pathogenesis: a bibliometric analysis.Frontiers in oncology · 2025Pooled it
- The origins and progression of pyloric metaplasia following gastric mucosal injury.Physiological reviews · 2026Review
- Disrupting SRSF10-dependent BCAT2 exon skipping reprograms tumor-associated macrophages and enhances anti-PD-1 efficacy in gastric cancer.Cell death & disease · 2026Article
- Regulation of STK38 by autophagy governs YAP1 activity during paligenosis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Multidimensional single-cell analysis reveals immune dysfunction and inflammatory response in lymphatic malformations.Protein & cell · 2026Article
- Multimerin1 and not Galectin-8 tempers WNT signaling to promote gastric chief cell differentiation.Scientific reports · 2026Article
- Evidence that injury can causebioRxiv : the preprint server for biology · 2026Article
- Recent advances in spasmolytic polypeptide expressing metaplasia research.World journal of gastrointestinal oncology · 2026Review
- Paligenosis: dual potential of mature cell plasticity in regeneration and tumorigenesis.MedScience · 2026Review
- Endoscopic and histopathological phenotypes of early gastric neoplasia: toward an integrative host-response framework.Frontiers in oncology · 2026Review
- Glycolytic reprogramming in precancerous lesions of gastric cancer progression: pathogenesis and therapeutic potential.Frontiers in oncology · 2026Review
- Targeting ferroptosis inInternational journal of oncology · 2026Review
- Epithelial WNT secretion drives niche escape of developing gastric cancer.Molecular cancer · 2025Article
- Multimerin1, not Galectin-8, Promotes Gastric Chief Cell Differentiation by Tempering WNT Signaling.bioRxiv : the preprint server for biology · 2025Article
- Research advancements and evaluation of multifactor-induced murine models for gastric cancer.Animal models and experimental medicine · 2025Review
- Revolutionizing Gastric Cancer Prevention: Novel Insights on Gastric Mucosal Inflammation-Cancer Transformation and Chinese Medicine.Chinese journal of integrative medicine · 2025Review
- Dissecting cross-lineage tumourigenesis under p53 inactivation through single-cell multi-omics and spatial transcriptomics.Clinical and translational medicine · 2025Article
- Cathartocytosis: Jettisoning of cellular material during reprogramming of differentiated cells.Cell reports · 2025Article
- Single-cell transcriptomic profiling uncovers cellular complexity and microenvironment in gastric tumorigenesis associated with Helicobacter pylori.Journal of advanced research · 2025Article
- Chronic Cigarette Smoke Exposure Masks Pathological Features of Helicobacter pylori Infection While Promoting Tumor Initiation.Cancer prevention research (Philadelphia, Pa.) · 2025Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 3 countries.
Funding
Abstract
BACKGROUND AND
aimsIn stomach, metaplasia can arise from differentiated chief cells that become mitotic via paligenosis, a stepwise program. In paligenosis, mitosis initiation requires reactivation of the cellular energy hub mTORC1 after initial mTORC1 suppression by DNA damage induced transcript 4 (DDIT4 aka REDD1). Here, we use DDIT4-deficient mice and human cells to study how metaplasia increases tumorigenesis risk.
methodsA tissue microarray of human gastric tissue specimens was analyzed by immunohistochemistry for DDIT4. C57BL/6 mice were administered combinations of intraperitoneal injections of high-dose tamoxifen (TAM) to induce spasmolytic polypeptide-expressing metaplasia (SPEM) and rapamycin to block mTORC1 activity, and N-methyl-N-nitrosourea (MNU) in drinking water to induce spontaneous gastric tumors. Stomachs were analyzed for proliferation, DNA damage, and tumor formation. CRISPR/Cas9-generated DDIT4
resultsDDIT4 was expressed in normal gastric chief cells in mice and humans and decreased as chief cells became metaplastic. Paligenotic Ddit4
conclusionsDuring injury-induced metaplastic proliferation, failure of licensing mTORC1 reactivation correlates with increased proliferation of cells harboring DNA damage, as well as increased tumor formation and growth in mice and humans.
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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.