ArticleCell death & disease2025
Tumor-derived PRMT1 suppresses macrophage antitumor activity by inhibiting cGAS/STING signaling in gastric cancer cells.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Reprogramming of cell death in gastric cancer: From molecular mechanisms to therapeutic potential (Review).International journal of molecular medicine · 2026Review
- Discovery of a non-canonical TREM2-S100A9 axis that drives pro-tumorigenic macrophage polarization and sensitizes ovarian clear cell carcinoma to IL-17 blockade.Cell death discovery · 2026Article
- Targeting the Cyclic GMP-AMP Synthase-Stimulator of Interferon Genes Pathway: An Emerging Therapeutic Strategy for Digestive Diseases.Clinical and translational gastroenterology · 2026Review
- Protein arginine methyltransferases in cancer: mechanisms, functions, and therapeutic opportunities.Journal of biomedical science · 2026Review
- Baicalin suppresses colorectal cancer proliferation and induces M1 polarization of tumor-associated macrophages by promoting proteasomal degradation of HK2.Frontiers in immunology · 2026Article
- Decoding the PTM code of cGAS-STING in gastric cancer: from innate DNA sensing to precision combination therapy.Frontiers in immunology · 2026Review
- Mitochondria: from powerhouses of cells to hubs in antitumor immunity.Frontiers in immunology · 2026Review
- PRMT1 in Health and Disease: Emerging Perspectives From Molecular Mechanisms to Therapeutic Strategies.MedComm · 2025Review
- The Role of Protein Arginine Methylation as a Post-Translational Modification in Cellular Homeostasis and Disease.Biology · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Gastric cancer (GC) is a common and aggressive malignancy worldwide. Increasing evidence has shown that epigenetic changes are closely related to the development of cancer and tumor-associated macrophages. Here, we report that PRMT1 is a key immunosuppressive factor in GC. PRMT1 is upregulated in GC and promotes tumor progression. PRMT1 knockdown in GC leads to the activation of the cGAS/STING pathway through the enhancement of dsDNA aggregation, which subsequently increases IFN-β secretion. Notably, after PRMT1 knockdown, M1-like tumor-associated macrophage (TAM) infiltration increased, whereas M2-like TAM infiltration decreased in vivo and in vitro. After the targeted inhibition of STING by siRNA or H151, the improvement in the progression of GC caused by PRMT1 knockdown decreased, and the changes in macrophage polarization were reversed. Furthermore, we found that PRMT1 knockdown in GC affects the STAT pathway in TAMs, inducing changes in their polarization and promoting GC apoptosis by enhancing IFN-β secretion through the cGAS/STING pathway. In summary, our findings revealed that PRMT1 knockdown inhibits the cGAS/STING pathway in GC, which produces type I IFNs to promote the polarization of M1-like macrophages in the tumor microenvironment.
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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.