Evidence map›Paper›PMID 28967907›Full record

ArticleOncogene2018

TRIM31 is upregulated in hepatocellular carcinoma and promotes disease progression by inducing ubiquitination of TSC1-TSC2 complex.

P Guo, X Ma, W Zhao, W Huai, T Li, Y Qiu, Y Zhang, L Han

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.

  1. [Advances of TRIM superfamily proteins in chronic liver disease and hepatocellular carcinoma].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2022
    Pooled it
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7 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

P GuoDepartment of Immunology, Shandong University School of Basic Medical Sciences, Jinan 250012, China.
X MaDepartment of Immunology, Shandong University School of Basic Medical Sciences, Jinan 250012, China.
W ZhaoDepartment of Immunology, Shandong University School of Basic Medical Sciences, Jinan 250012, China.
W HuaiDepartment of Immunology, Shandong University School of Basic Medical Sciences, Jinan 250012, China.
T LiDepartment of Gastroenterology, Provincial Hospital Affiliated with Shandong University, Jinan 250021, China.
Y QiuDepartment of Immunology, Shandong University School of Basic Medical Sciences, Jinan 250012, China.
Y ZhangDepartment of Immunology, Shandong University School of Basic Medical Sciences, Jinan 250012, China.
L HanDepartment of Immunology, Shandong University School of Basic Medical Sciences, Jinan 250012, China.
Shandong University · CNShandong Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tripartite motif (TRIM) 31 is a member of the tripartite motif-containing protein family, and TRIM family proteins are involved in a broad range of biological and pathological processes. However, the role of TRIM31 in hepatocellular carcinoma (HCC) progression is not known. Here we demonstrated that TRIM31 expression was significantly upregulated in liver cancer tissues compared with paired distal non-cancerous liver tissues from HCC patients, and its overexpression was significantly correlated with advanced disease status. Both gain and loss of function assay verified that TRIM31 promoted the malignant behaviors of HCC cells through overactivation of mammalian target of rapamycin complex1 (mTORC1) pathway. We further demonstrated that TRIM31 exerted its oncogenic effect by directly interacting with the tuberous sclerosis complex (TSC) 1 and TSC2 complex, the upstream suppressor of mTORC1 pathway, and promoting the E3 ligase-mediated K48-linked ubiquitination and degradation of this complex. In conclusion, this study demonstrated TRIM31 could promote HCC progression by targeting TSC1-TSC2 complex for degradation and further overactivating mTORC1 pathway. Thus, it revealed a novel molecular mechanism of HCC progression and indicated a potential therapeutic strategy against HCC by targeting TRIM31.

Indexed as

AnimalsCarcinoma, HepatocellularCell Line, TumorCohort StudiesDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansLiverLiver NeoplasmsMaleMechanistic Target of Rapamycin Complex 1Mice, Inbred BALB CMice, NudeMiddle AgedMutagenesis, Site-DirectedMechanistic Target of Rapamycin Complex 1RNA, Small InterferingTRIM31 protein, humanTripartite Motif ProteinsTSC1 protein, humanTsc1 protein, mouseTSC2 protein, humanTsc2 protein, mouseTuberous Sclerosis Complex 1 ProteinTuberous Sclerosis Complex 2 ProteinTumor Suppressor ProteinsUbiquitin-Protein Ligases

Identifiers

PMID28967907
OpenAlexW2763579433

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.