Evidence map›Paper›PMID 17325666›Full record

ArticleOncogene2007

Xeroderma pigmentosum group C gene expression is predominantly regulated by promoter hypermethylation and contributes to p53 mutation in lung cancers.

Y-H Wu, J-H Tsai Chang, Y-W Cheng, T-C Wu, C-Y Chen, H Lee

Abstract read
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In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

32 citing papers in PubMed, 53 citations in OpenAlex.

  1. Higher Levels ofMedical sciences (Basel, Switzerland) · 2026
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  4. Association ofmedRxiv : the preprint server for health sciences · 2023
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  16. Genetic Evidence for XPC-KRAS Interactions During Lung Cancer Development.Journal of genetics and genomics = Yi chuan xue bao · 2015
    Article
  17. Review
  18. Article
  19. Article
  20. Article
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

6 authors at 3 institutions in 1 country.

Y-H WuInstitute of Medical and Molecular Toxicology, Chung Shan Medical University, Taichung, Taiwan, ROC.
J-H Tsai Chang
Y-W Cheng
T-C Wu
C-Y Chen
H Lee
Chung Shan Medical University · TWChina Medical University · TWChung Shan Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reduced DNA repair capability is associated with developing lung cancer, especially in nonsmokers. XPC participates in the initial recognition of DNA damage during the DNA nucleotide excision repair process. We hypothesize that inactivation of XPC by promoter hypermethylation may play an important role in the reduction of DNA repair capability to cause p53 mutation during lung carcinogenesis. In this report we demonstrate that hypermethylation of 17 CpG islands between -175 and -1 of the XPC promoter correlates very well with XPC expression levels in eight lung cancer cell lines. When cells with hypermethylated XPC promoters were treated with the demethylating agent 5-aza-2'-deoxycytidine, XPC expression was de-repressed. Interestingly, XPC hypermethylation was found in 4 of 5 (80%) lung cancer cell lines harbored p53 mutation, but not observed in two lung cancer cells which had a wild-type p53 gene. Among the analysis of the hypermethylation status of 158 lung tumors, XPC hypermethylation is more common in nonsmokers (39 of 94, 41%) than in smokers (14 of 64, 22%; P=0.010). Additionally, XPC hypermethylation is more often with G --> T or G --> C mutations in the p53 gene. To verify whether XPC inactivation is involved in the occurrence of p53 mutation, XPC gene of A549 cells was knockdown by a small interference RNA and then XPC-inactivated cells were treated with benzo[a]pynrene for different passages. Surprisingly, G --> T mutation in p53 gene at codon 215 was indeed detected in XPC-inactivated A549 cells of passages 15 and confirmed by loss of transcription activity of mdm2. These results show that hypermethylation of the XPC promoter may play a crucial role in XPC inactivation, which may partly contribute to the occurrence of p53 mutations during lung tumorigenesis, especially nonsmokers.

Indexed as

DNA MethylationMutationAgedAzacitidineBase SequenceBlotting, WesternCell Line, TumorCpG IslandsDecitabineDNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticHumansLuciferasesLung NeoplasmsMaleAzacitidineDecitabineDNA-Binding ProteinsLuciferasesMDM2 protein, humanProto-Oncogene Proteins c-mdm2Recombinant Fusion ProteinsTumor Suppressor Protein p53XPC protein, human

Identifiers

PMID17325666
OpenAlexW1969918392

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.