Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
September 10, 2025Cell Death and DiseaseOpen Access

Tumor-derived PRMT1 suppresses macrophage antitumor activity by inhibiting cGAS/STING signaling in gastric cancer cells

View Full Paper
Ask AI
Bookmark
Share

Authors

HWHui WangHNHe NieXZXiaoyi Zhao

Discussion

Loading...

Member takes

Overview

Targeted PRMT1 knockdown activates cGAS/STING signaling in gastric cancer cells, suggesting novel immunotherapeutic strategies.

Key Points

  • PRMT1 knockdown significantly enhances cGAS/STING pathway activation, increasing IFN-β secretion.
  • M1-like tumor-associated macrophages (TAMs) increased and M2-like TAMs decreased following PRMT1 knockdown.
  • Inhibition of STING reversed the positive effects on GC progression seen with PRMT1 knockdown.
  • PRMT1 influences macrophage polarization and apoptosis in gastric cancer by altering the STAT signaling pathway.

Cite This Study

Wang et al. (2025) studied this question.

synapsesocial.com/papers/68c24317b210217d647a5dachttps://doi.org/10.1038/s41419-025-07960-y
View Full Paper
Ask AI
Bookmark
Share

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Identification of a stromal immunosuppressive barrier orchestrated by SPP1+/C1QC+ macrophages and CD8+ exhausted T cells driving gastric cancer immunotherapy resistance2025
  2. 2DNMT inhibition epigenetically restores the cGAS-STING pathway and activates RIG-I/MDA5-MAVS to enhance antitumor immunity2025 · 25 citations
  3. 3TRIM6 ablation reverses ICB resistance in MSS gastric cancer by unleashing cGAS-STING-dependent antitumor immunity2025
  4. 4Tumors with microsatellite instability upregulate TREX1 to escape antitumor immunity2025
  5. 5Identification of an M1 Macrophages-Related Signature for Predicting the Survival and Therapeutic Response in Gastric Cancer.2025