Evidence map›Paper›PMID 42210578›Full record

ArticleAutophagy2026

MEN1/menin deficiency suppresses hepatocellular carcinogenesis via disrupting mitophagy-mediated mitochondrial homeostasis.

Chaochun Chen, Dafang Yu, Dekun Tang, Mengyuan Liu, Jiamei Zhu, Xuyan Wang, Guixue Dan, Lan Chen, Shumei Tang, Qianting Tian and 7 more

Abstract read
In one paragraph

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

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

17 authors.

Chaochun ChenDepartment of Hepatobiliary Surgery, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, P. R. China.
Dafang YuDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guian, Guizhou, P. R. China.ORCID 0009-0001-8490-0596
Dekun TangDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guian, Guizhou, P. R. China.
Mengyuan LiuDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guian, Guizhou, P. R. China.
Jiamei ZhuDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guian, Guizhou, P. R. China.ORCID 0009-0003-5230-3740
Xuyan WangDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guian, Guizhou, P. R. China.
Guixue DanDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guian, Guizhou, P. R. China.
Lan ChenDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guian, Guizhou, P. R. China.
Shumei TangDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guian, Guizhou, P. R. China.
Qianting TianDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guian, Guizhou, P. R. China.
Houmei WangDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guian, Guizhou, P. R. China.
Fuxue MengPrecision Medicine Research Institute, Guizhou Medical University, Guizhou, P. R. China.
Tuo ZhangDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guian, Guizhou, P. R. China.
Bing GuoGuizhou Provincial Key Laboratory of Pathogenesis and Drug Research on Common Chronic Diseases, Guizhou Medical University, Guian, Guizhou, P. R. China.
Tengxiang ChenDepartment of Hepatobiliary Surgery, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, P. R. China.ORCID 0000-0001-8730-8515
Haiyang LiDepartment of Hepatobiliary Surgery, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, P. R. China.ORCID 0000-0003-0015-5750
Bangming JinDepartment of Hepatobiliary Surgery, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, P. R. China.ORCID 0000-0002-2997-5587

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a highly lethal liver cancer with complex pathogenesis intertwined with metabolic and mitochondrial dysfunction. MEN1/menin is a protein with context-dependent functions in liver diseases. While MEN1 has been linked to HCC progression and mitochondrial homeostasis, its precise regulatory mechanism in these processes remains incompletely understood. Here, we report that MEN1 localizes to the outer mitochondrial membrane (OMM) in HCC cells, which is mediated by its N-terminal mitochondrial targeting sequence and the TOMM20 translocase complex. In a genetically engineered DEN- and CCl

Indexed as

CarcinogenesisCarcinoma, HepatocellularHomeostasisLiver NeoplasmsMitochondriaMitophagyProto-Oncogene ProteinsAnimalsCell Line, TumorHumansMaleMiceMitochondrial MembranesMitochondrial Precursor Protein Import Complex ProteinsMitochondrial Precursor Protein Import Complex ProteinsProto-Oncogene ProteinsEnergy metabolismMEN1 genemitochondrial fissionmitochondrial MEN1mitophagy

Identifiers

PMID42210578
PMCPMC13618852

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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.