Evidence map›Paper›PMID 39920289›Full record

ArticleOncogene2025

PRSS23-eIF4E-c-Myc axis promotes gastric tumorigenesis and progression.

Xiaodong Zhou, Zixiang Guo, Yating Pan, Sicheng Yang, Runwei Yan

Abstract read
PubMed Publisher
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Xiaodong Zhou *Department of Gastroenterology, Jiangxi Provincial Key Laboratory of Digestive Diseases, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Zixiang Guo *Department of Gastroenterology, Jiangxi Provincial Key Laboratory of Digestive Diseases, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Yating Pan *Department of Gastroenterology, Jiangxi Provincial Key Laboratory of Digestive Diseases, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Sicheng YangDepartment of Gastroenterology, Jiangxi Provincial Key Laboratory of Digestive Diseases, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Runwei YanDepartment of Gastroenterology, Jiangxi Provincial Key Laboratory of Digestive Diseases, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China. Runwei_Yan0202@hotmail.com.ORCID http://orcid.org/0000-0002-1762-136X

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81960444Natural Science Foundation of Jiangxi Province (Jiangxi Province Natural Science Foundation) 20212BAB206037
6 · The paper itself

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.

Indexed as

CarcinogenesisEukaryotic Initiation Factor-4EProto-Oncogene Proteins c-mycStomach NeoplasmsAnimalsCell Line, TumorCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeMiddle AgedPrognosisEIF4E protein, humanEukaryotic Initiation Factor-4EMYC protein, humanProto-Oncogene Proteins c-myc

Identifiers

PMID39920289

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.