Evidence map›Paper›PMID 38514606›Full record

ArticleNature communications2024

The EIF3H-HAX1 axis increases RAF-MEK-ERK signaling activity to promote colorectal cancer progression.

Huilin Jin, Xiaoling Huang, Qihao Pan, Ning Ma, Xiaoshan Xie, Yue Wei, Fenghai Yu, Weijie Wen, Boyu Zhang, Peng Zhang and 6 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
6.5field-weighted citation impact, top 2% of its field
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

20 citing papers in PubMed, 28 citations in OpenAlex.

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  16. PJA2 Suppresses Colorectal Cancer Progression by Controlling HDAC2 Degradation and Stability.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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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

16 authors at 2 institutions in 1 country.

Huilin Jin *Department of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Xiaoling Huang *Department of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Qihao Pan *Guangdong Provincial Key laboratory of Colorectal and Pelvic Floor Disease, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Ning MaDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Xiaoshan XieDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Yue WeiDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Fenghai YuDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Weijie WenDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Boyu ZhangDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Peng ZhangDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Xijie ChenDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Jie WangDepartment of Radiation Oncology, Dalian Municipal Central Hospital, Dalian, China.
Ran-Yi LiuState Key Laboratory of Oncology in South China & Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.ORCID http://orcid.org/0000-0002-3986-0177
Junzhong LinState Key Laboratory of Oncology in South China & Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.ORCID http://orcid.org/0000-0003-4038-1939
Xiangqi MengDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. mengxq3@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-6407-6122
Mong-Hong LeeDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. limh33@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0001-8675-8215
Sun Yat-sen University · CNDalian Municipal Central Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81630072National Natural Science Foundation of China (National Science Foundation of China) 82273133
6 · The paper itself

Abstract

Eukaryotic initiation translation factor 3 subunit h (EIF3H) plays critical roles in regulating translational initiation and predicts poor cancer prognosis, but the mechanism underlying EIF3H tumorigenesis remains to be further elucidated. Here, we report that EIF3H is overexpressed in colorectal cancer (CRC) and correlates with poor prognosis. Conditional Eif3h deletion suppresses colorectal tumorigenesis in AOM/DSS model. Mechanistically, EIF3H functions as a deubiquitinase for HAX1 and stabilizes HAX1 via antagonizing βTrCP-mediated ubiquitination, which enhances the interaction between RAF1, MEK1 and ERK1, thereby potentiating phosphorylation of ERK1/2. In addition, activation of Wnt/β-catenin signaling induces EIF3H expression. EIF3H/HAX1 axis promotes CRC tumorigenesis and metastasis in mouse orthotopic cancer model. Significantly, combined targeting Wnt and RAF1-ERK1/2 signaling synergistically inhibits tumor growth in EIF3H-high patient-derived xenografts. These results uncover the important roles of EIF3H in mediating CRC progression through regulating HAX1 and RAF1-ERK1/2 signaling. EIF3H represents a promising therapeutic target and prognostic marker in CRC.

Indexed as

Colorectal NeoplasmsMAP Kinase Signaling SystemAdaptor Proteins, Signal TransducingAnimalsCarcinogenesisCell Line, TumorCell ProliferationCell Transformation, NeoplasticEukaryotic Initiation Factor-3Gene Expression Regulation, NeoplasticHumansMiceMitogen-Activated Protein Kinase KinasesPhosphorylationWnt Signaling PathwayAdaptor Proteins, Signal TransducingEukaryotic Initiation Factor-3HAX1 protein, humanMitogen-Activated Protein Kinase Kinases

Identifiers

PMID38514606
PMCPMC10957977
OpenAlexW4393032116

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.