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      NETO2 Is Deregulated in Breast, Prostate, and Colorectal Cancer and Participates in Cellular Signaling

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          Abstract

          The NETO2 gene (neuropilin and tolloid-like 2) encodes a protein that acts as an accessory subunit of kainate receptors and is predominantly expressed in the brain. Upregulation of NETO2 has been observed in several tumors; however, its role in tumorigenesis remains unclear. In this study, we investigated NETO2 expression in breast, prostate, and colorectal cancer using quantitative PCR (qPCR), as well as the effect of shRNA-mediated NETO2 silencing on transcriptome changes in colorectal cancer cells. In the investigated tumors, we observed both increased and decreased NETO2 mRNA levels, presenting no correlation with the main clinicopathological characteristics. In HCT116 cells, NETO2 knockdown resulted in the differential expression of 17 genes and 2 long non-coding RNAs (lncRNAs), associated with the upregulation of circadian rhythm and downregulation of several cancer-associated pathways, including Wnt, transforming growth factor (TGF)-β, Janus kinase (JAK)-signal transducer and activator of transcription (STAT), mitogen-activated protein kinase (MAPK), and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathways. Furthermore, we demonstrated the possibility to utilize a novel model organism, short-lived fish Nothobranchius furzeri, for evaluating NETO2 functions. The ortholog neto2b in N. furzeri demonstrated a high similarity in nucleotide and amino acid sequences with human NETO2, as well as was characterized by stable expression in various fish tissues. Collectively, our findings demonstrate the deregulation of NETO2 in the breast, prostate, and colorectal cancer and its participation in the tumor development primarily through cellular signaling.

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          Most cited references35

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          Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2

          In comparative high-throughput sequencing assays, a fundamental task is the analysis of count data, such as read counts per gene in RNA-seq, for evidence of systematic changes across experimental conditions. Small replicate numbers, discreteness, large dynamic range and the presence of outliers require a suitable statistical approach. We present DESeq2, a method for differential analysis of count data, using shrinkage estimation for dispersions and fold changes to improve stability and interpretability of estimates. This enables a more quantitative analysis focused on the strength rather than the mere presence of differential expression. The DESeq2 package is available at http://www.bioconductor.org/packages/release/bioc/html/DESeq2.html. Electronic supplementary material The online version of this article (doi:10.1186/s13059-014-0550-8) contains supplementary material, which is available to authorized users.
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            Wnt signaling in cancer

            Wnt signaling is one of the key cascades regulating development and stemness, and has also been tightly associated with cancer. The role of Wnt signaling in carcinogenesis has most prominently been described for colorectal cancer, but aberrant Wnt signaling is observed in many more cancer entities. Here, we review current insights into novel components of Wnt pathways and describe their impact on cancer development. Furthermore, we highlight expanding functions of Wnt signaling for both solid and liquid tumors. We also describe current findings how Wnt signaling affects maintenance of cancer stem cells, metastasis and immune control. Finally, we provide an overview of current strategies to antagonize Wnt signaling in cancer and challenges that are associated with such approaches.
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              TGFbeta in Cancer.

              The transforming growth factor beta (TGFbeta) signaling pathway is a key player in metazoan biology, and its misregulation can result in tumor development. The regulatory cytokine TGFbeta exerts tumor-suppressive effects that cancer cells must elude for malignant evolution. Yet, paradoxically, TGFbeta also modulates processes such as cell invasion, immune regulation, and microenvironment modification that cancer cells may exploit to their advantage. Consequently, the output of a TGFbeta response is highly contextual throughout development, across different tissues, and also in cancer. The mechanistic basis and clinical relevance of TGFbeta's role in cancer is becoming increasingly clear, paving the way for a better understanding of the complexity and therapeutic potential of this pathway.
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                Author and article information

                Contributors
                Journal
                Front Genet
                Front Genet
                Front. Genet.
                Frontiers in Genetics
                Frontiers Media S.A.
                1664-8021
                10 December 2020
                2020
                : 11
                : 594933
                Affiliations
                [1] 1Center for Precision Genome Editing and Genetic Technologies for Biomedicine, Engelhardt Institute of Molecular Biology, Russian Academy of Sciences , Moscow, Russia
                [2] 2A. N. Severtsov Institute of Ecology and Evolution, Russian Academy of Sciences , Moscow, Russia
                [3] 3National Medical Research Radiological Center, Ministry of Health of the Russian Federation , Moscow, Russia
                [4] 4National Medical Research Center for Obstetrics, Gynecology and Perinatology Named After Academician V.I. Kulakov, Ministry of Health of the Russian Federation , Moscow, Russia
                Author notes

                Edited by: Yuriy L. Orlov, I.M. Sechenov First Moscow State Medical University, Russia

                Reviewed by: Stanislav Rybtsov, University of Edinburgh, United Kingdom; Elvira Galieva, Novosibirsk State University, Russia

                *Correspondence: Anastasiya V. Snezhkina, leftger@ 123456rambler.ru
                Anna V. Kudryavtseva, rhizamoeba@ 123456mail.ru

                These authors have contributed equally to this work

                This article was submitted to Computational Genomics, a section of the journal Frontiers in Genetics

                Article
                10.3389/fgene.2020.594933
                7758476
                33362854
                bdf5a8d8-261c-4e2c-bf45-b2ca6398bbb3
                Copyright © 2020 Fedorova, Snezhkina, Lipatova, Pavlov, Kobelyatskaya, Guvatova, Pudova, Savvateeva, Ishina, Demidova, Volchenko, Trofimov, Sukhikh, Krasnov and Kudryavtseva.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 14 August 2020
                : 19 November 2020
                Page count
                Figures: 4, Tables: 1, Equations: 0, References: 35, Pages: 8, Words: 0
                Funding
                Funded by: Ministry of Science and Higher Education of the Russian Federation 10.13039/501100012190
                Award ID: 075-15-2019-1660
                Categories
                Genetics
                Original Research

                Genetics
                neto2,breast cancer,prostate cancer,colorectal cancer,fish model
                Genetics
                neto2, breast cancer, prostate cancer, colorectal cancer, fish model

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