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

8.5
来源: Nature
发布时间: 2025-08-27 03:46
摘要:

PRMT1, an epigenetic regulator, is found to suppress macrophage antitumor activity in gastric cancer by inhibiting the cGAS/STING signaling pathway. Its knockdown promotes M1 macrophage polarization and enhances the antitumor immune response, indicating its potential as a therapeutic target in gastric cancer treatment.

原文: 查看原文

价值分投票

评分标准

新闻价值分采用0-10分制,综合考虑新闻的真实性、重要性、时效性、影响力等多个维度。 评分越高,表示该新闻的价值越大,越值得关注。

价值维度分析

domain_focus

1.0分+1.0

business_impact

0.8分+0.8

scientific_rigor

1.5分+1.5

timeliness_innovation

1.5分+1.5

investment_perspective

2.5分+2.5

market_value_relevance

1.0分+1.0

team_institution_background

0.5分+0.5

technical_barrier_competition

1.0分+1.0

关键证据

PRMT1 knockdown leads to increased infiltration of M1-like macrophages.
Activation of cGAS/STING signaling enhances antitumor immunity.
PRMT1 is associated with poor prognosis in gastric cancer patients.

真实性检查

AI评分总结

PRMT1, an epigenetic regulator, is found to suppress macrophage antitumor activity in gastric cancer by inhibiting the cGAS/STING signaling pathway. Its knockdown promotes M1 macrophage polarization and enhances the antitumor immune response, indicating its potential as a therapeutic target in gastric cancer treatment.

评论讨论

发表评论