Evidence map›Paper›PMID 40691141›Full record

ArticleCell death discovery2025

EIF3B stabilizes MAP2K2 to activate the ERK pathway and promote the progression of laryngeal squamous cell carcinoma.

Jie Tan, Xueshi Li, Yuguang Wang, Lin Wang, Xingguo Zhao, Yixu Wang, Meng Cui

Abstract read
In one paragraph

Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. mFrontiers in cell and developmental biology · 2026
    Review
  3. Article
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

7 authors.

Jie Tan *Department of Otorhinolaryngology Head and Neck Surgery, Peking University People's Hospital, Peking University, Beijing, PR China.ORCID http://orcid.org/0000-0002-3011-7715
Xueshi Li *Department of Otorhinolaryngology Head and Neck Surgery, Peking University People's Hospital, Peking University, Beijing, PR China.
Yuguang WangDepartment of Otorhinolaryngology Head and Neck Surgery, Peking University People's Hospital, Peking University, Beijing, PR China.
Lin WangDepartment of Otorhinolaryngology Head and Neck Surgery, Peking University People's Hospital, Peking University, Beijing, PR China.
Xingguo ZhaoDepartment of Otorhinolaryngology Head and Neck Surgery, Peking University People's Hospital, Peking University, Beijing, PR China.
Yixu WangDepartment of Otorhinolaryngology Head and Neck Surgery, Peking University People's Hospital, Peking University, Beijing, PR China.
Meng CuiDepartment of Head and Neck Thyroid, Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, PR China. cmsky83@163.com.ORCID http://orcid.org/0000-0003-3115-8794

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To elucidate the role of eukaryotic translation initiation factor 3 subunit B (EIF3B) in laryngeal squamous cell carcinoma (LSCC) progression and its regulatory mechanism. Integrated bioinformatics analysis (GEO, TCGA), immunohistochemistry (IHC), lentiviral-mediated gene knockdown/overexpression, co-immunoprecipitation (Co-IP), Western blotting (WB), and in vivo xenograft models were employed. Clinically, our findings revealed an upregulation of EIF3B expression in LSCC, with its abnormally high levels significantly correlating with poor survival outcomes among patients. Functionally, ablation of EIF3B potently inhibited cancer cell proliferation, colony formation, and migratory abilities. Mechanistically, EIF3B stabilized MAP2K2 via direct interaction with its P3 domain, inhibiting VHL-mediated ubiquitination at K169. Notably, MAP2K2 kinase activity was essential for EIF3B-driven ERK phosphorylation and downstream oncogenic signaling. Moreover, EIF3B overexpression accelerated tumor growth in xenograft models, which was rescued by MAP2K2 knockdown. In Conclusion, EIF3B promotes LSCC progression by stabilizing MAP2K2, activating the ERK/MAPK pathway, and disrupting VHL-mediated proteostasis. Targeting the EIF3B-MAP2K2 axis may offer therapeutic strategies for LSCC.

Identifiers

PMID40691141
PMCPMC12280010

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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 OpenQuestion graph.