Evidence map›Paper›PMID 27471552›Full record

ArticleJournal of Cancer2016

The Expression Levels of XLF and Mutant P53 Are Inversely Correlated in Head and Neck Cancer Cells.

Sizhe Feng, Ramin Rabii, Guobiao Liang, Chenxi Song, Wei Chen, Mian Guo, Xuezhong Wei, Diana Messadi, Shen Hu

Open access · goldAbstract read
In one paragraph

Article in Journal of Cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 28% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Sox11 promotes head and neck cancer progression via the regulation of SDCCAG8.Journal of experimental & clinical cancer research : CR · 2019
    Article
  6. Review
  7. 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 2 countries.

Sizhe Feng1. School of Dentistry and Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA 90095, USA; 2. North Hospital, Shenyang, China.
Ramin Rabii1. School of Dentistry and Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA 90095, USA.
Guobiao Liang2. North Hospital, Shenyang, China.
Chenxi Song1. School of Dentistry and Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA 90095, USA.
Wei Chen1. School of Dentistry and Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA 90095, USA.
Mian Guo1. School of Dentistry and Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA 90095, USA.
Xuezhong Wei2. North Hospital, Shenyang, China.
Diana Messadi1. School of Dentistry and Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA 90095, USA.
Shen Hu1. School of Dentistry and Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA 90095, USA.
University of California, Los Angeles · USShenyang 242 Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

XRCC4-like factor (XLF), also known as Cernunnos, is a protein encoded by the human NHEJ1 gene and an important repair factor for DNA double-strand breaks. In this study, we have found that XLF is over-expressed in HPV(+) versus HPV(-) head and neck squamous cell carcinoma (HNSCC) and significantly down-regulated in the HNSCC cell lines expressing high level of mutant p53 protein versus those cell lines harboring wild-type TP53 gene with low p53 protein expression. We have also demonstrated that Werner syndrome protein (WRN), a member of the NHEJ repair pathway, binds to both mutant p53 protein and NHEJ1 gene promoter, and siRNA knockdown of WRN leads to the inhibition of XLF expression in the HNSCC cells. Collectively, these findings suggest that WRN and p53 are involved in the regulation of XLF expression and the activity of WRN might be affected by mutant p53 protein in the HNSCC cells with aberrant TP53 gene mutations, due to the interaction of mutant p53 with WRN. As a result, the expression of XLF in these cancer cells is significantly suppressed. Our study also suggests that XLF is over-expressed in HPV(+) HNSCC with low expression of wild type p53, and might serve as a potential biomarker for HPV(+) HNSCC. Further studies are warranted to investigate the mechanisms underlying the interactive role of WRN and XLF in NHEJ repair pathway.

Indexed as

biomarkerHNSCCHPVmutant p53XLF

Identifiers

PMID27471552
PMCPMC4964120
OpenAlexW2468707073

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.