Evidence map›Paper›PMID 25929687›Full record

ArticleBMC cancer2015

Wilms' tumor gene 1 regulates p63 and promotes cell proliferation in squamous cell carcinoma of the head and neck.

Xingru Li, Sofia Ottosson, Sihan Wang, Emma Jernberg, Linda Boldrup, Xiaolian Gu, Karin Nylander, Aihong Li

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Xingru LiDepartment of Medical Biosciences, Clinical Chemistry, Umeå University, By 6 M, 2nd floor, Umeå, 90185, Sweden. xingru.li@medbio.umu.se.
Sofia OttossonDepartment of Medical Biosciences, Clinical Chemistry, Umeå University, By 6 M, 2nd floor, Umeå, 90185, Sweden. soot0002@student.umu.se.
Sihan WangDepartment of Medical Biosciences, Clinical Chemistry, Umeå University, By 6 M, 2nd floor, Umeå, 90185, Sweden. sihan.wang@medbio.umu.se.
Emma JernbergDepartment of Medical Biosciences, Pathology, Umeå University, By 6 M, 2nd floor, Umeå, 90185, Sweden. emma.jernberg@medbio.umu.se.
Linda BoldrupDepartment of Medical Biosciences, Pathology, Umeå University, By 6 M, 2nd floor, Umeå, 90185, Sweden. linda.boldrup@medbio.umu.se.
Xiaolian GuDepartment of Medical Biosciences, Pathology, Umeå University, By 6 M, 2nd floor, Umeå, 90185, Sweden. xiaolian.gu@medbio.umu.se.
Karin NylanderDepartment of Medical Biosciences, Pathology, Umeå University, By 6 M, 2nd floor, Umeå, 90185, Sweden. karin.nylander@medbio.umu.se.
Aihong LiDepartment of Medical Biosciences, Clinical Chemistry, Umeå University, By 6 M, 2nd floor, Umeå, 90185, Sweden. aihong.li@medbio.umu.se.
Umeå University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWilms' tumor gene 1 (WT1) can act as a suppressor or activator of tumourigenesis in different types of human malignancies. The role of WT1 in squamous cell carcinoma of the head and neck (SCCHN) is not clear. Overexpression of WT1 has been reported in SCCHN, suggesting a possible oncogenic role for WT1. In the present study we aimed at investigating the function of WT1 and its previously identified protein partners p63 and p53 in the SCCHN cell line FaDu.

methodsSilencing RNA (siRNA) technology was applied to knockdown of WT1, p63 and p53 in FaDu cells. Cell proliferation was detected using MTT assay. Chromatin immunoprecipitation (ChIP)/PCR analysis was performed to confirm the effect of WT1 on the p63 promoter. Protein co-immunoprecipitation (co-IP) was used to find protein interaction between WT1 and p53/p63. Microarray analysis was used to identify changes of gene expression in response to knockdown of either WT1 or p63. WT1 RNA level was detected using real-time quantitative PCR (RT-qPCR) in patients with SCCHN.

resultsWe found that WT1 and p63 promoted cell proliferation, while mutant p53 (R248L) possessed the ability to suppress cell proliferation. We reported a novel positive correlation between WT1 and p63 expression. Subsequently, p63 was identified as a WT1 target gene. Furthermore, expression of 18 genes involved in cell proliferation, cell cycle regulation and DNA replication was significantly altered by downregulation of WT1 and p63 expression. Several known WT1 and p63 target genes were affected by WT1 knockdown. Protein interaction was demonstrated between WT1 and p53 but not between WT1 and p63. Additionally, high WT1 mRNA levels were detected in SCCHN patient samples.

conclusionsOur findings suggest that WT1 and p63 act as oncogenes in SCCHN, affecting multiple genes involved in cancer cell growth.

Indexed as

Carcinoma, Squamous CellCell Line, TumorCell ProliferationGenes, Wilms TumorHead and Neck NeoplasmsHumansMembrane ProteinsSquamous Cell Carcinoma of Head and NeckCKAP4 protein, humanMembrane Proteins

Identifiers

PMID25929687
PMCPMC4421988
OpenAlexW2128092349

What OpenQuestion holds

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LicenceCC BY
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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.