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      Dysregulated genes and miRNAs in the apoptosis pathway in colorectal cancer patients

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          Abstract

          Apoptosis is genetically regulated and involves intrinsic and extrinsic pathways. We examined 133 genes within these pathways to identify whether they are expressed differently in colorectal carcinoma (CRC) and normal tissue (N = 217) and if they are associated with similar differential miRNA expression. Gene expression data (RNA-Seq) and miRNA expression data (Agilent Human miRNA Microarray V19.0) were generated. We focused on dysregulated genes with a fold change (FC) of > 1.50 or < 0.67, that were significant after adjustment for multiple comparisons. miRNA:mRNA seed-region matches were determined. Twenty-three genes were significantly downregulated (FC < 0.67) and 18 were significantly upregulated (FC > 1.50). Of these 41 genes, 11 were significantly associated with miRNA differential expression. BIRC5 had the greatest number of miRNA associations (14) and the most miRNAs with a seed-region match (10). Four of these matches, miR-145-5p, miR-150-5p, miR-195-5p, and miR-650, had a negative beta coefficient. CSF2RB was associated with ten total miRNAs (five with a seed-region match, and one miRNA, miR-92a-3p, with a negative beta coefficient). Of the three miRNAs associated with CTSS, miR-20b-5p, and miR-501-3p, had a seed-region match and a negative beta coefficient between miRNA:mRNA pairs. Several miRNAs that were associated with dysregulated gene expression, seed-region matches, and negative beta coefficients also were associated with CRC-specific survival. Our data suggest that miRNAs could influence several apoptosis-related genes. BIRC5, CTSS, and CSF2R all had seed-region matches with miRNAs that would favor apoptosis. Our study identifies several miRNA associated with apoptosis-related genes, that if validated, could be important therapeutic targets.

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          The online version of this article (10.1007/s10495-018-1451-1) contains supplementary material, which is available to authorized users.

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          Most cited references28

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          Controlling the False Discovery Rate: A Practical and Powerful Approach to Multiple Testing

          Yoav Benjamini, Yosef Hochberg (1995)
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            Structure and function of the feed-forward loop network motif.

            S Mangan, U Alon (2011)
            Engineered systems are often built of recurring circuit modules that carry out key functions. Transcription networks that regulate the responses of living cells were recently found to obey similar principles: they contain several biochemical wiring patterns, termed network motifs, which recur throughout the network. One of these motifs is the feed-forward loop (FFL). The FFL, a three-gene pattern, is composed of two input transcription factors, one of which regulates the other, both jointly regulating a target gene. The FFL has eight possible structural types, because each of the three interactions in the FFL can be activating or repressing. Here, we theoretically analyze the functions of these eight structural types. We find that four of the FFL types, termed incoherent FFLs, act as sign-sensitive accelerators: they speed up the response time of the target gene expression following stimulus steps in one direction (e.g., off to on) but not in the other direction (on to off). The other four types, coherent FFLs, act as sign-sensitive delays. We find that some FFL types appear in transcription network databases much more frequently than others. In some cases, the rare FFL types have reduced functionality (responding to only one of their two input stimuli), which may partially explain why they are selected against. Additional features, such as pulse generation and cooperativity, are discussed. This study defines the function of one of the most significant recurring circuit elements in transcription networks.
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              miRTarBase 2016: updates to the experimentally validated miRNA-target interactions database

              Chih-Hung Chou, Nai-Wen Chang, Sirjana Devi Shrestha … (2015)
              MicroRNAs (miRNAs) are small non-coding RNAs of approximately 22 nucleotides, which negatively regulate the gene expression at the post-transcriptional level. This study describes an update of the miRTarBase (http://miRTarBase.mbc.nctu.edu.tw/) that provides information about experimentally validated miRNA-target interactions (MTIs). The latest update of the miRTarBase expanded it to identify systematically Argonaute-miRNA-RNA interactions from 138 crosslinking and immunoprecipitation sequencing (CLIP-seq) data sets that were generated by 21 independent studies. The database contains 4966 articles, 7439 strongly validated MTIs (using reporter assays or western blots) and 348 007 MTIs from CLIP-seq. The number of MTIs in the miRTarBase has increased around 7-fold since the 2014 miRTarBase update. The miRNA and gene expression profiles from The Cancer Genome Atlas (TCGA) are integrated to provide an effective overview of this exponential growth in the miRNA experimental data. These improvements make the miRTarBase one of the more comprehensively annotated, experimentally validated miRNA-target interactions databases and motivate additional miRNA research efforts.
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                Author and article information

                Contributors
                Martha L. Slattery:
                ORCID: http://orcid.org/0000-0002-1655-6543
                801-585-6955 , marty.slattery@hsc.utah.edu
                Journal
                Journal ID (nlm-ta): Apoptosis
                Journal ID (iso-abbrev): Apoptosis
                Title: Apoptosis
                Publisher: Springer US (New York )
                ISSN (Print): 1360-8185
                ISSN (Electronic): 1573-675X
                Publication date (Electronic): 7 March 2018
                Publication date PMC-release: 7 March 2018
                Publication date (Print): 2018
                Volume: 23
                Issue: 3
                Pages: 237-250
                Affiliations
                [1 ]ISNI 0000 0001 2193 0096, GRID grid.223827.e, Department of Medicine, , University of Utah, ; 383 Colorow, Salt Lake City, UT 84108 USA
                [2 ]ISNI 0000 0000 9957 7758, GRID grid.280062.e, Division of Research, , Kaiser Permanente Northern California, ; Oakland, CA USA
                [3 ]ISNI 0000 0001 2193 0096, GRID grid.223827.e, Department of Pathology, , University of Utah, ; Salt Lake City, UT USA
                Author information
                http://orcid.org/0000-0002-1655-6543
                Article
                Publisher ID: 1451
                DOI: 10.1007/s10495-018-1451-1
                PMC ID: 5856858
                PubMed ID: 29516317
                SO-VID: b1acf777-277f-45c8-b5d6-66a0fd903424
                Copyright © © The Author(s) 2018
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100000054, National Cancer Institute;
                Award ID: CA163683
                Award Recipient :
                Categories
                Subject: Original Paper
                Custom metadata
                issue-copyright-statement © Springer Science+Business Media, LLC, part of Springer Nature 2018

                ScienceOpen disciplines: Molecular biology
                Keywords: apoptosis,colorectal cancer,mirna,mrna,birc5,ctss
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: apoptosis, colorectal cancer, mirna, mrna, birc5, ctss

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