ArticleOncology letters2019
Investigation of miRNA- and lncRNA-mediated competing endogenous RNA network in cholangiocarcinoma.
Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- MicroRNAs Associated with IgLON Cell Adhesion Molecule Expression.Current issues in molecular biology · 2024Review
- LINC00844 suppresses tumor progression and predicts survival outcomes through inhibiting miR-19a-5p in cholangiocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Article
- Protein profiling reveals potential isomiR-associated cross-talks among RNAs in cholangiocarcinoma.Computational and structural biotechnology journal · 2021Article
- MiR-144: A New Possible Therapeutic Target and Diagnostic/Prognostic Tool in Cancers.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cholangiocarcinoma (CCA) is a biliary malignancy which is prone to lymphatic metastasis and has a high mortality rate. This disease lacks effective therapeutic targets and prognostic molecular biomarkers. The aim of the current study was to investigate differentially expressed genes and elucidate their association with CCA and the underlying mechanisms of action. mRNAs, long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) obtained from 36 CCA samples and nine normal samples from The Cancer Genome Atlas were integrated. Subsequently, 1,095 differentially expressed (DE) mRNAs and 75 DE miRNAs were identified using a threshold of |log2 fold change|>2 and an adjusted P<0.01. Weighted gene co-expression network analysis was used to identify the DEmRNAs that could be key target genes in CCA. A total of 12 hub DEmRNAs were identified as targetable genes. Furthermore, the hub DEmRNAs-DElncRNAs pairs were identified using the miRTarBase and miRcode databases. Cytoscape software was used to construct and visualize the protein-protein interactions and the competing endogenous RNA network. Survival time analysis and correlation analysis were used to further evaluate the hub genes. The results obtained in the current study suggested that spalt like transcription factor 3 and OPCML intronic transcript 1 may serve an important role in the development and progression of CCA.
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Registered trials
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