Evidence map›Paper›PMID 41668065›Full record

ArticleRespiratory research2026

EIF3B regulates the cell cycle of lung adenocarcinoma cells by activating the GTSE1 mediated ERK/MAPK pathway.

Yingru Xing, Zhao Feng, Ying Zhang, Jing Dai, Zichao Bao, Cheng Tao, Jingjing Dai, Haizhou Wang

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In one paragraph

Article in Respiratory research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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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.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Yingru Xing *School of Medicine, Anhui University of Science and Technology, Huainan, 232001, China.
Zhao Feng *Department of Breast and Thyroid Surgery, The First Affiliated Hospital, Anhui University of Science and Technology, Huainan, 232001, China.
Ying ZhangSchool of Medicine, Anhui University of Science and Technology, Huainan, 232001, China.
Jing DaiSchool of Medicine, Anhui University of Science and Technology, Huainan, 232001, China.
Zichao BaoSchool of Medicine, Anhui University of Science and Technology, Huainan, 232001, China.
Cheng TaoSchool of Medicine, Anhui University of Science and Technology, Huainan, 232001, China.
Jingjing DaiDepartment of Medical Laboratory, The Affiliated Huai'an NO.1 People's Hospital of Naniing Medical University, Huaian, Jiangsu, 223001, China. hayydaijj@njmu.edu.cn.
Haizhou WangDepartment of Blood Transfusion, Shanghai Pudong New Area People's Hospital, Shanghai, 201299, China. wanghzpdph@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo preliminary explore the expression pattern, clinical significance, and potential molecular mechanism of EIF3B in lung adenocarcinoma (LUAD), and to provide preliminary evidence for its potential as a diagnostic and prognostic biomarker and therapeutic target (to be further verified by subsequent experiments).

methodsLUAD data were obtained from multiple databases, and various statistical methods were used to analyze the correlation between EIF3B expression and clinical characteristics as well as prognosis. Cell experiments (transfection, wound healing, etc.), mouse subcutaneous tumor models, and Western blotting were combined to explore the function and mechanism of EIF3B.

resultsEIF3B was highly expressed in LUAD tissues, which was associated with advanced staging and poor prognosis, with a diagnostic AUC value of 0.911. Knockdown of EIF3B inhibited the proliferation and migration of cancer cells, while overexpression promoted these processes. EIF3B activated the ERK/MAPK pathway by positively regulating GTSE1, thereby regulating cell cycle proteins. In mouse experiments, knockdown of EIF3B reduced tumor volume by approximately 60% and tumor weight by approximately 55% without affecting health.

conclusionEIF3B drives LUAD progression through the “EIF3B-GTSE1-ERK/MAPK-cell cycle” axis and has dual potential as a diagnostic and therapeutic target.

Indexed as

Adenocarcinoma of LungCell CycleEukaryotic Initiation Factor-3Lung NeoplasmsMAP Kinase Signaling SystemAnimalsCell Line, TumorCell ProliferationFemaleHumansMaleMiceMice, NudeEIF3B protein, humanEukaryotic Initiation Factor-3Cell cycleERK/MAPKEukaryotic initiation factor 3 subunit b (EIF3B)G2 and s phase expressed 1(GTSE1)Lung adenocarcinoma (LUAD)

Identifiers

PMID41668065
PMCPMC12998141

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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.