Evidence map›Paper›PMID 31571992›Full record

ArticleCancer management and research2019

UBE2T promotes proliferation via G2/M checkpoint in hepatocellular carcinoma.

Li-Li Liu, Ji-Min Zhu, Xiang-Nan Yu, Hai-Rong Zhu, Xuan Shi, Enkhnaran Bilegsaikhan, Hong-Ying Guo, Jian Wu, Xi-Zhong Shen

Open access · goldAbstract read
In one paragraph

Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 62 citations in OpenAlex.

  1. Ubiquitin-conjugating Enzymes in Cancer.International journal of biological sciences · 2026
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  7. The role of ubiquitin-conjugating enzyme in the process of spermatogenesis.Reproductive biology and endocrinology : RB&E · 2024
    Review
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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

9 authors at 1 institution in 2 countries.

Li-Li Liu *Department of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.
Ji-Min Zhu *Department of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.ORCID 0000-0002-2150-473X
Xiang-Nan YuDepartment of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.
Hai-Rong ZhuDepartment of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.
Xuan ShiDepartment of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.
Enkhnaran BilegsaikhanDepartment of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.
Hong-Ying GuoDepartment of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.
Jian WuDepartment of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.
Xi-Zhong ShenDepartment of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.
Shanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGrowing evidence suggests that the ubiquitin-proteasome system is involved in the pathogenesis and recurrence of hepatocellular carcinoma (HCC); yet, little is known about the role of ubiquitin-conjugating enzyme E2T (UBE2T) in HCC. MATERIALS AND

methodsUBE2T levels were detected in HCC tissues and hepatoma cell lines using quantitative reserve transcriptase-polymerase chain reaction and Western blot analysis. Next, the changes of phenotypes after UBE2T knockdown or overexpression were evaluated using in vitro methods. Finally, the mechanism of UBE2T in HCC was tested using ex vivo and in vivo methods.

resultsIn the present study, we reported that UBE2T mRNA and protein levels were significantly upregulated in HCC tissues compared to adjacent non-tumor tissues. Additionally, suppression of UBE2T expression inhibited proliferation, colony formation, tumorigenesis, migration, and invasion of hepatoma cells, whereas UBE2T overexpression led to the opposite outcomes. Moreover, suppression of UBE2T expression resulted in an increase in G2/M phase and a decrease in the percentage of cells in G1 phase, which indicated a cell cycle arrest at the G2/M phase. In contrast, the percentage of cells in G2/M phase decreased following UBE2T overexpression. Further study indicated that UBE2T regulated the G2/M transition by modulating cyclin B1 and cyclin-dependent kinase 1.

conclusionTaken together, the findings of the present study uncover biological functions of UBE2T in hepatoma cells, and delineate preliminary molecular mechanisms of UBE2T in modulating HCC development and progression.

Indexed as

cell cyclehepatocellular carcinomaUBE2Tubiquitination

Identifiers

PMID31571992
PMCPMC6750879
OpenAlexW2973092482

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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.