Evidence map›Paper›PMID 35224960›Full record

ArticleZhongguo fei ai za zhi = Chinese journal of lung cancer2022

PRKCDBP Methylation is a Potential and Promising Candidate Biomarker for Non-small Cell Lung Cancer.

Jing Li, Lin Qi, Mingfang Zhang, Caiyun Yao, Jinan Feng, Zhonghua Zheng, Chujia Chen, Shiwei Duan, Yuanlin Qi

Open access · greenAbstract read
In one paragraph

Article in Zhongguo fei ai za zhi = Chinese journal of lung cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.2field-weighted citation impact, top 54% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 2 citations in OpenAlex.

  1. Pooled it
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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

9 authors at 2 institutions in 1 country.

Jing Li *School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China.
Lin Qi *School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China.
Mingfang Zhang *School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China.
Caiyun YaoSchool of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China.
Jinan FengSchool of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China.
Zhonghua ZhengMedical Genetics Center, School of Medicine, Ningbo University, Ningbo 315211, China.
Chujia ChenMedical Genetics Center, School of Medicine, Ningbo University, Ningbo 315211, China.
Shiwei DuanMedical Genetics Center, School of Medicine, Ningbo University, Ningbo 315211, China.
Yuanlin QiSchool of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China.
Fujian Medical University · CNNingbo University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe occurrence and development of lung cancer are closely linked to epigenetic modification. Abnormal DNA methylation in the CpG island region of genes has been found in many cancers. Protein kinase C delta binding protein (PRKCDBP) is a potential tumor suppressor and its epigenetic changes are found in many human malignancies. This study investigated the possibility of PRKCDBP methylation as a potential biomarker for non-small cell lung cancer (NSCLC).

methodsWe measured the methylation levels of PRKCDBP in the three groups of NSCLC tissues. Promoter activity was measured by the dual luciferase assay, with 5'-aza-deoxycytidine to examine the effect of demethylation on the expression level of PRKCDBP.

resultsThe methylation levels of PRKCDBP in tumor tissues and 3 cm para-tumor were higher than those of distant (>10 cm) non-tumor tissues. Receiver operating characteristic (ROC) curve analysis between tumor tissues and distant non-tumor tissues showed that the area under the line (AUC) was 0.717. Dual luciferase experiment confirmed that the promoter region was able to promote gene expression. Meanwhile, in vitro methylation of the fragment (PRKCDBP_Me) could significantly reduce the promoter activity of the fragment. Demethylation of 5'-aza-deoxycytidine in lung cancer cell lines A549 and H1299 showed a significant up-regulation of PRKCDBP mRNA levels.

conclusionsPRKCDBP methylation is a potential and promising candidate biomarker for non-small cell lung cancer.

Indexed as

Carcinoma, Non-Small-Cell LungDNA MethylationLung NeoplasmsBiomarkersCell Line, TumorGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsPromoter Regions, GeneticBiomarkersCAVIN3 protein, humanIntracellular Signaling Peptides and ProteinsDNA methylationLung neoplasmsPRKCDBP

Identifiers

PMID35224960
PMCPMC8913286
OpenAlexW4214711565

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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.