Loading
Life sciences · Journal article
The Faseb Journal · September 19, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
ABSTRACT Cancer‐associated fibroblasts (CAFs) are pivotal stromal component in tumor microenvironment (TME) and participate in regulating tumor development and progression via exosomes (exos) mediated intercommunication. However, the intricate mechanism underlying the exosomal miRNAs from CAFs in gastric cancer (GC) tumorigenesis remains ambiguous. Herein, we found that miR‐4435 was highly expressed in both CAFs‐ derived exos and GC tissues and was associated with TNM stage as well as tumor size in GC patients. Additionally, inhibition of miR‐4435 remarkably restricted GC proliferation, migration, and invasion in vitro and in vivo; whereas facilitating ferroptosis in GC cells. Moreover, miR‐4435 could bind with the downstream target NDUFA10 mRNA and was shown to silence NDUFA10 expression. Importantly, exosomal miR‐4435 derived from CAFs could suppress CD8 + T cells effector function, contributing to immune resistance, while knockdown of miR‐4435 in CAFs‐exo could foster CD8 + T cells effector function and enhanced the sensitivity of anti‐PD‐1 therapy in GC. Collectively, exosomal miR‐4435 derived from CAFs suppress ferroptosis and CD8 + T cell effector function in GC via mediating NDUFA10. Our results highlight exos‐transfered miR‐4435 as a potential therapeutic target in GC.