ArticleNPJ systems biology and applications2020
Signatures of co-deregulated genes and their transcriptional regulators in colorectal cancer.
Article in NPJ systems biology and applications, 2020. 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 21 papers.
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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
21 citing papers in PubMed, 28 citations in OpenAlex.
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- Bioinformatics screening of colorectal-cancer causing molecular signatures through gene expression profiles to discover therapeutic targets and candidate agents.BMC medical genomics · 2023Article
- CircNDST1 promotes papillary thyroid cancer progression via its interaction with CSNK2A1 to activate the PI3K-Akt pathway and epithelial-mesenchymal transition.Journal of endocrinological investigation · 2023Article
- Mechanistic insights into zearalenone-accelerated colorectal cancer in mice using integrative multi-omics approaches.Computational and structural biotechnology journal · 2023Article
- Signatures of Co-Deregulated Genes and Their Transcriptional Regulators in Lung Cancer.International journal of molecular sciences · 2022Article
- Therapeutic Targeting of Cancer Stem Cells Prevents Resistance of Colorectal Cancer Cells to MEK Inhibition.ACS pharmacology & translational science · 2022Article
- Exosomal Components and Modulators in Colorectal Cancer: Novel Diagnosis and Prognosis Biomarkers.Biomedicines · 2021Review
- CTSE Overexpression Is an Adverse Prognostic Factor for Survival among Rectal Cancer Patients Receiving CCRT.Life (Basel, Switzerland) · 2021Article
- Review
- Artificial Intelligence in Cancer Research and Precision Medicine.Cancer discovery · 2021Review
- Identification of Novel Kinase-Transcription Factor-mRNA-miRNA Regulatory Network in Nasopharyngeal Carcinoma by Bioinformatics Analysis.International journal of general medicine · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The deregulated genes in colorectal cancer (CRC) vary significantly across different studies. Thus, a systems biology approach is needed to identify the co-deregulated genes (co-DEGs), explore their molecular networks, and spot the major hub proteins within these networks. We reanalyzed 19 GEO gene expression profiles to identify and annotate CRC versus normal signatures, single-gene perturbation, and single-drug perturbation signatures. We identified the co-DEGs across different studies, their upstream regulating kinases and transcription factors (TFs). Connectivity Map was used to identify likely repurposing drugs against CRC within each group. The functional changes of the co-upregulated genes in the first category were mainly associated with negative regulation of transforming growth factor β production and glomerular epithelial cell differentiation; whereas the co-downregulated genes were enriched in cotranslational protein targeting to the membrane. We identified 17 hub proteins across the co-upregulated genes and 18 hub proteins across the co-downregulated genes, composed of well-known TFs (MYC, TCF3, PML) and kinases (CSNK2A1, CDK1/4, MAPK14), and validated most of them using GEPIA2 and HPA, but also through two signature gene lists composed of the co-up and co-downregulated genes. We further identified a list of repurposing drugs that can potentially target the co-DEGs in CRC, including camptothecin, neostigmine bromide, emetine, remoxipride, cephaeline, thioridazine, and omeprazole. Similar analyses were performed in the co-DEG signatures in single-gene or drug perturbation experiments in CRC. MYC, PML, CDKs, CSNK2A1, and MAPKs were common hub proteins among all studies. Overall, we identified the critical genes in CRC and we propose repurposing drugs that could be used against them.
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