Evidence map›Paper›PMID 38773518›Full record

ArticleJournal of translational medicine2024

UBXN1 promotes liver tumorigenesis by regulating mitochondrial homeostasis.

Kun Jiao, Guiqin Xu, Yun Liu, Zhaojuan Yang, Lvzhu Xiang, Zehong Chen, Chen Xu, You Zuo, Zhibai Wu, Ningqian Zheng and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

13 authors.

Kun Jiao *State Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, 200240, China.
Guiqin Xu *State Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200240, China.
Yun LiuState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200240, China.
Zhaojuan YangState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200240, China.
Lvzhu XiangState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200240, China.
Zehong ChenState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200240, China.
Chen XuState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200240, China.
You ZuoState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200240, China.
Zhibai WuState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200240, China.
Ningqian ZhengState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200240, China.
Wangjie XuLaboratory Animal Center, Instrumental Analysis Center, Shanghai Jiao Tong University, Shanghai, 200240, China.
Li ZhangState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200240, China. zhangli@shsci.org.
Yongzhong LiuState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, 200240, China. liuyzg@shsci.org.ORCID 0000-0002-1477-116X

Funding

Innovative Research Team of High-level Local University in Shanghai Innovative Research Team of High-level Local University in ShanghaiNational Natural Science Foundation of China 81902373National Natural Science Foundation of China 81972579National Natural Science Foundation of China 82273002National Natural Science Foundation of China 82273005Natural Science Foundation of Shanghai Municipality 20ZR1454100Shanghai Rising-Star Program 21QA1408400State Key Laboratory of Systems Medicine for Cancer JY2193State Key Laboratory of Systems Medicine for Cancer JY2224State Key Laboratory of Systems Medicine for Cancer zz-94-2304State Key Laboratory of Systems Medicine for Cancer zz-RCPY-23-05
6 · The paper itself

Abstract

backgroundThe maintenance of mitochondrial homeostasis is critical for tumor initiation and malignant progression because it increases tumor cell survival and growth. The molecular events controlling mitochondrial integrity that facilitate the development of hepatocellular carcinoma (HCC) remain unclear. Here, we report that UBX domain-containing protein 1 (UBXN1) hyperactivation is essential for mitochondrial homeostasis and liver tumorigenesis.

methodsOncogene-induced mouse liver tumor models were generated with the Sleeping Beauty (SB) transposon delivery system. Assessment of HCC cell growth in vivo and in vitro, including tumour formation, colony formation, TUNEL and FACS assays, was conducted to determine the effects of UBXN1 on HCC cells, as well as the involvement of the UBXN1-prohibitin (PHB) interaction in mitochondrial function. Coimmunoprecipitation (Co-IP) was used to assess the interaction between UBXN1 and PHB. Liver hepatocellular carcinoma (LIHC) datasets and HCC patient samples were used to assess the expression of UBXN1.

resultsUBXN1 expression is commonly upregulated in human HCCs and mouse liver tumors and is associated with poor overall survival in HCC patients. UBXN1 facilitates the growth of human HCC cells and promotes mouse liver tumorigenesis driven by the NRas/c-Myc or c-Myc/shp53 combination. UBXN1 interacts with the inner mitochondrial membrane protein PHB and sustains PHB expression. UBXN1 inhibition triggers mitochondrial damage and liver tumor cell apoptosis.

conclusionsUBXN1 interacts with PHB and promotes mitochondrial homeostasis during liver tumorigenesis.

Indexed as

CarcinogenesisCarcinoma, HepatocellularHomeostasisLiver NeoplasmsMitochondriaProhibitinsAdaptor Proteins, Signal TransducingAnimalsApoptosisCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMiceProtein BindingRepressor ProteinsAdaptor Proteins, Signal TransducingPHB protein, humanProhibitinsRepressor ProteinsUBXN1 protein, humanApoptosisHepatocellular carcinomaMitochondrial homeostasisPHBUBXN1

Identifiers

PMID38773518
PMCPMC11110256

What Socratic holds

Textmetadata
LicenceCC BY
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.