Glypican‐3 Upregulated by <scp>YTHDF1</scp> in an <scp>m6A</scp> ‐Dependent Manner Interacts With <scp>MUL1</scp> to Repress <scp>HSF1</scp> Ubiquitination Degradation, Boost <scp>CD276</scp> Transcription, and Mediate Immune Escape in Gastric Cancer

T cells through the MUL1/HSF1/CD276 axis, mediating GC tumor immune escape. YTHDF1 upregulates the expression of GPC3 in GC in an m6A-dependent manner. GPC3 interacts with MUL1 to depress the ubiquitination degradation of HSF1, thereby upregulating the immune checkpoint CD276 and affecting GC immune escape.

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Publication Details

Journal
The FASEB Journal
Published
2026-04-07
DOI
https://doi.org/10.1096/fj.202503106r
Primary Topic
RNA modifications and cancer
Type
article
Field-Weighted Citation Impact
0.00
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article

Glypican‐3 Upregulated by YTHDF1 in an m6A ‐Dependent Manner Interacts With MUL1 to Repress HSF1 Ubiquitination Degradation, Boost CD276 Transcription, and Mediate Immune Escape in Gastric Cancer

Dinuo Li, Chen Li
The FASEB Journal
RNA modifications and cancer
article

Glypican‐3 Upregulated by YTHDF1 in an m6A ‐Dependent Manner Interacts With MUL1 to Repress HSF1 Ubiquitination Degradation, Boost CD276 Transcription, and Mediate Immune Escape in Gastric Cancer

Dinuo Li, Chen Li
article en

Abstract

T cells through the MUL1/HSF1/CD276 axis, mediating GC tumor immune escape. YTHDF1 upregulates the expression of GPC3 in GC in an m6A-dependent manner. GPC3 interacts with MUL1 to depress the ubiquitination degradation of HSF1, thereby upregulating the immune checkpoint CD276 and affecting GC immune escape.

The FASEB JournalVol. 40(7)
Affiliated Hospital of Jining Medical University (CN), Jinzhou Medical University (CN)
Openalex Percentile: Top 22%
RNA modifications and cancer
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