ArticleFrontiers in genetics2021
Molecular Characteristics of Choledochal Cysts in Children: Transcriptome Sequencing.
Article in Frontiers in genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Current status of the biliary tract malformation.World journal of clinical pediatrics · 2024Review
- Review
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Corrections and comments
- Erratum issued
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A choledochal cyst (CC) is a common congenital biliary disease in children, yet the underlying molecular bases for the cystic and fusiform clinical subtypes are unknown. RNA sequencing (RNA-seq) has been performed on 22 high-quality CC samples, including 12 cystic CC and 10 fusiform CC samples, to search for molecular features. Weighted gene co-expression network analysis (WGCNA) was performed to identify key modules associated with clinical subtypes. Bioinformatic analyses were conducted to elucidate potential mechanisms. Then, we constructed protein-protein interaction (PPI) networks to identify candidate hub genes related to CC. Finally, we used the support vector machine (SVM) to eliminate redundant features and screen out the hub genes. The selected gene expression was determined in CC patients through quantitative real-time polymerase chain reaction (PCR). A total of 6,463 genes were found to be aberrantly expressed between cystic CC and fusiform CC. Twelve co-expression modules that correlated with clinical subtypes of CC were identified and assigned representative colors. Among the 12 modules, the blue module was considered the key module. Two functionally distinct sets of dysregulated genes have been identified in two major subtypes, metabolism-related genes in cystic CC and immune-related genes in fusiform CC. A total of 20 candidate hub genes that were correlated with clinical subtypes were found in the blue module. In addition, we found ERBB2 and WNT11 that have not been studied in CC and verified their differential expression in CC through quantitative real-time PCR experiments. For the first time, we have described the transcriptome characteristics of CC. These results suggest that cystic CC and fusiform CC have different molecular mechanisms. The bi-omics-identified novel candidate genes and pathways might be helpful for personalized treatment and are of great clinical significance for CC.
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