Evidence map›Paper›PMID 35728518›Full record

ArticleIntervirology2022

Identification and Verification of Ubiquitin D as a Gene Associated with Hepatitis C Virus-Induced Hepatocellular Carcinoma.

Huanqin Li, Shumin Liu, Yun Lin, Xiongfei Shi, Na Du, Jing Yao, Ruiyang Liu, Yan Du, Kai Yang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Intervirology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 26% 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

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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 2 institutions in 1 country.

Huanqin LiDepartment of Clinical Laboratory, First Affiliated Hospital of Yunnan University of Chinese Medicine, Kunming, China.
Shumin LiuDepartment of Clinical Laboratory, First Affiliated Hospital of Kunming Medical University, Kunming, China.
Yun LinDepartment of Clinical Laboratory, First Affiliated Hospital of Yunnan University of Chinese Medicine, Kunming, China.
Xiongfei ShiDepartment of Clinical Laboratory, First Affiliated Hospital of Yunnan University of Chinese Medicine, Kunming, China.
Na DuDepartment of Clinical Laboratory, First Affiliated Hospital of Yunnan University of Chinese Medicine, Kunming, China.
Jing YaoDepartment of Clinical Laboratory, First Affiliated Hospital of Yunnan University of Chinese Medicine, Kunming, China.
Ruiyang LiuDepartment of Clinical Laboratory, First Affiliated Hospital of Yunnan University of Chinese Medicine, Kunming, China.
Yan DuDepartment of Clinical Laboratory, First Affiliated Hospital of Kunming Medical University, Kunming, China.
Kai YangDepartment of Clinical Laboratory, First Affiliated Hospital of Kunming Medical University, Kunming, China.
Yunnan University · CNKunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAccumulated studies have suggested that hepatitis C virus (HCV) infection is one of the leading causes for hepatocellular carcinoma (HCC). However, the mechanisms underlying the effect of HCV on the occurrence of HCC are still poorly understood.

methodsHCV infection datasets (GSE82177 and GSE17856) and HCC datasets (The Cancer Genome Atlas Liver Hepatocellular Carcinoma and GSE89377) were downloaded from Gene Expression Omnibus or TCGA for analysis. The common differentially expressed genes in the above four datasets were identified by R software. The expression of ubiquitin D (UBD) in HCV-infected HepG2 cells was detected by RT-qPCR and Western blot, respectively. The interaction between NS3 and p53 was detected by co-immunoprecipitation. The influence of UBD on the proliferation and migration ability of HepG2 cells was evaluated by CCK-8 and wound healing assay, respectively.

resultsUBD was upregulated in both HCV-infected samples and HCC samples. HCV NS3 interacted with p53 and inhibited its expression. HCV NS3-induced UBD promoted the proliferation and migration of HepG2 cells.

conclusionOur results suggest that HCV NS3-induced UBD is positively correlated with the development of HCV-related HCC during HCV infection. Targeting UBD could be a potential strategy for preventing and treating HCV-induced HCC.

Indexed as

Carcinoma, HepatocellularHepatitis CLiver NeoplasmsUbiquitinsHumansTumor Suppressor Protein p53Tumor Suppressor Protein p53UBD protein, humanUbiquitinsHepatitis C virusLiver hepatocellular carcinomaNS3p53Ubiquitin D

Identifiers

PMID35728518
PMCPMC9677847
OpenAlexW4283271361

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.