ArticleOncogene2025
PRSS23-eIF4E-c-Myc axis promotes gastric tumorigenesis and progression.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- PRSS23 promotes ovarian cancer peritoneal dissemination independent of protease activity.The Journal of biological chemistry · 2026Article
- Eukaryotic initiation factors: central factor associating mRNA translational plasticity during neuropathic pain progression.Frontiers in neurology · 2025Review
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Authors and funding
5 authors.
Funding
Abstract
Gastric cancer is one of the most common malignant tumors. Our previous study showed that PRSS23 expression is increased in human gastric cancer tissues and PRSS23 knockdown inhibits gastric cancer cell growth. This current study aims to uncover the mechanism underlying PRSS23's involvement in gastric tumorigenesis and progression. We established that PRSS23 influences gastric cancer growth both in vitro and in vivo by modulating the eIF4E-c-Myc axis (eIF4E, p-eIF4E, 4EBP1, p-4EBP1, and c-Myc). Our investigation revealed that PRSS23 interacts with eIF4E via its trypsin domain, while eIF4E binds to PRSS23 through the amino acid residue S209, as confirmed by co-IP and immunofluorescence assays. Multiplexed immunofluorescence assay demonstrated a significant elevation of PRSS23 and p-4EBP1 levels in 232 paired gastric cancer tissues. Moreover, in 49 patients exhibiting relatively high PRSS23 expression, the levels of eIF4E-c-Myc axis-related proteins were increased. Importantly, higher PRSS23 expression correlated significantly with increased lymph node metastasis and advanced clinical staging, leading to poorer patient prognosis. These results highlight the role of upregulated PRSS23 in promoting gastric tumorigenesis and progression by activating the eIF4E-c-Myc axis, underscoring the PRSS23-eIF4E-c-Myc axis as a promising therapeutic target for gastric cancer.
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Registered trials
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