Evidence map›Paper›PMID 24013223›Full record

ArticleOncogene2014

Mutations in 3'-long terminal repeat of HERV-W family in chromosome 7 upregulate syncytin-1 expression in urothelial cell carcinoma of the bladder through interacting with c-Myb.

H Yu, T Liu, Z Zhao, Y Chen, J Zeng, S Liu, F Zhu

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 2 pooled it
1.3field-weighted citation impact, top 20% 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

78 citing papers in PubMed, 2 syntheses or guidelines pooled it, 87 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  18. Review
  19. Cell-cell fusion in cancer: The next cancer hallmark?The international journal of biochemistry & cell biology · 2024
    Review
  20. Article

18 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

H YuDepartment of Medical Microbiology, School of Medicine, Wuhan University, Wuhan, China.
T LiuState Key Laboratory of Proteomics, Department of Neurobiology, Beijing Institute of Basic Medical Sciences, Beijing, China.ORCID 0000000317016618
Z ZhaoDepartment of Urology, Zhongnan Hospital, Wuhan University, Wuhan, China.
Y ChenDepartment of Medical Microbiology, School of Medicine, Wuhan University, Wuhan, China.
J ZengDepartment of Medical Microbiology, School of Medicine, Wuhan University, Wuhan, China.
S LiuState Key Laboratory of Proteomics, Department of Neurobiology, Beijing Institute of Basic Medical Sciences, Beijing, China.
F ZhuDepartment of Medical Microbiology, School of Medicine, Wuhan University, Wuhan, China.
Wuhan University · CNBeijing Proteome Research Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human endogenous retrovirus (HERV) accounts for ∼8% of the human genome. Recent studies have reported that multiple HERV genes and long terminal repeats (LTRs) are involved in human tumorigenesis. Here we demonstrated that HERV-W env (syncytin-1) was overexpressed in 75.6% (62/82) of urothelial cell carcinoma (UCC) tissues of the bladder compared with only 6.1% (5/82) of matched tumor-adjacent tissues (P<0.001). Syncytin-1 overexpression increased proliferation and viability of immortalized human uroepithelial cells. Colony-formation experiments and in-vivo tumor xenografts suggested that syncytin-1 overexpression had oncogenic potential. Syncytin-1 3'-LTR mutations (142T>C and 277A>G) were present in 87.8% (72/82) of UCC tissues. Normal 3'-LTR was found in 12.2% (10/82) of UCC tissues compared with 95.1% (78/82) of matched tumor-adjacent tissues (P<0.001). Interestingly, 3'-LTR mutations were significantly associated with syncytin-1 overexpression. Luciferase assay and expression analysis revealed that 3'-LTR mutations, especially the 142T>C mutation, enhanced the syncytin-1 promoter activity and expression. In-silico analysis, electrophoretic mobility shift assays and chromatin immunoprecipitation assays demonstrated the binding of c-Myb to 3'-LTRs when the mutations occurred. This alternative interaction was found to be dependent on 142T>C mutation. C-Myb activated syncytin-1 promoter activity and expression by binding to mutant 3'-LTRs. Taken together, these data indicate that syncytin-1 overexpression may be an indicator of UCC risk. The 3'-LTR mutations may upregulate syncytin-1 expression, enabling it to participate in UCC tumorigenesis and development by interacting with c-Myb.

Indexed as

AnimalsBase SequenceCarcinoma, Transitional CellCell ProliferationChromosomes, Human, Pair 7DNA Mutational AnalysisEndogenous RetrovirusesFemaleGene Expression Regulation, NeoplasticGene Products, envHumansMaleMiceMice, Inbred BALB CMice, NudeMiddle AgedGene Products, envPregnancy ProteinsProto-Oncogene Proteins c-mybsyncytin

Identifiers

PMID24013223
OpenAlexW1978753282

What OpenQuestion holds

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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.