Lecules are pervasively transcribed and roughly classified as antisense, based on their position relative to the protein-coding genes [5] and?2016 Sun et al. This 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. The Creative Commons Public Domain get GW 4064 Dedication waiver (http://creativecommons.org/publicdomain/ zero/1.0/) applies to the data made available in this article, unless otherwise stated.Sun et al. J Transl Med (2016) 14:Page 2 ofexhibit cis- or trans- regulatory capabilities for gene expression. Gene expression patterns indicate that these lncRNAs are implicated in diverse biological processes, including nuclear architecture, regulation of gene expression, immune surveillance, or embryonic stem cell pluripotency. Recently, evidence revealing the molecular mechanisms by which these RNA species function has provided some insight into the functional roles they may play in tumorigenesis [6]. Aberrant lncRNA expression participates in carcinogenesis by disrupting major biological processes, such as redirecting chromatin remodeling complexes or inactivating major tumor suppressor genes [6, 7]. Among these, PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27385778 LincRNA taurine up-regulated gene 1 (TUG1; also known as TI-227H; Linc00080; ncRNA00080) was originally identified as a transcript up-regulated by taurine and is found to be expressed in various human cancer cell lines and tumors [8]. Upregulation of the long noncoding RNA TUG1 promotes proliferation and migration of esophageal squamous cell carcinoma [9]. Downregulation of long non-coding RNA TUG1 inhibits osteosarcoma cell proliferation and promotes apoptosis [10]. However, the role of TUG1 in colorectal cancer remains unclear. This study was established due to our speculation that TUG1 may have roles to play in the CRC pathological process. Previously, research has found that the metastasis and invasion of cancer cells are common events that mediate changes in cellular behavior, and induce different steps in the metastatic cascade [11, 12]. One of the most crucial steps in the tumor cell metastatic cascade is the acquisition of invasive capabilities, including destroying cell ell junctions, degrading the cell matrix, and activating pathways that control the cytoskeletal dynamics of cancer cells. Over the past decade, cell and tumor biologists have identified the key role of epithelial-mesenchymal transition (EMT)-a biological process in which epithelial cells lose their polarity and transition into a mesenchymal phenotype-in cancer cell metastasis [13]. Evidence suggests that EMT enhances tumor cell invasion in response to environmental triggers, augments invasive functions, and also contributes to cell growth and survival [14, 15]. In preliminary experiments, we found that upregulated UTR1 expression in metastatic CRC cell lines predicted poor survival for CRC patients. This current study was designed to search the evidence supporting a role for TUG1 in the metastasis of CRC in representative CRC cell lines. We further attempted the preliminary exploration of the possible association of EMT-related gene expression by TUG1.AZD3759MedChemExpress AZD3759 patients who had undergone gastrointestinal surgery between 2008 and 2013 at t.Lecules are pervasively transcribed and roughly classified as antisense, based on their position relative to the protein-coding genes [5] and?2016 Sun et al. This 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. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/ zero/1.0/) applies to the data made available in this article, unless otherwise stated.Sun et al. J Transl Med (2016) 14:Page 2 ofexhibit cis- or trans- regulatory capabilities for gene expression. Gene expression patterns indicate that these lncRNAs are implicated in diverse biological processes, including nuclear architecture, regulation of gene expression, immune surveillance, or embryonic stem cell pluripotency. Recently, evidence revealing the molecular mechanisms by which these RNA species function has provided some insight into the functional roles they may play in tumorigenesis [6]. Aberrant lncRNA expression participates in carcinogenesis by disrupting major biological processes, such as redirecting chromatin remodeling complexes or inactivating major tumor suppressor genes [6, 7]. Among these, PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27385778 LincRNA taurine up-regulated gene 1 (TUG1; also known as TI-227H; Linc00080; ncRNA00080) was originally identified as a transcript up-regulated by taurine and is found to be expressed in various human cancer cell lines and tumors [8]. Upregulation of the long noncoding RNA TUG1 promotes proliferation and migration of esophageal squamous cell carcinoma [9]. Downregulation of long non-coding RNA TUG1 inhibits osteosarcoma cell proliferation and promotes apoptosis [10]. However, the role of TUG1 in colorectal cancer remains unclear. This study was established due to our speculation that TUG1 may have roles to play in the CRC pathological process. Previously, research has found that the metastasis and invasion of cancer cells are common events that mediate changes in cellular behavior, and induce different steps in the metastatic cascade [11, 12]. One of the most crucial steps in the tumor cell metastatic cascade is the acquisition of invasive capabilities, including destroying cell ell junctions, degrading the cell matrix, and activating pathways that control the cytoskeletal dynamics of cancer cells. Over the past decade, cell and tumor biologists have identified the key role of epithelial-mesenchymal transition (EMT)-a biological process in which epithelial cells lose their polarity and transition into a mesenchymal phenotype-in cancer cell metastasis [13]. Evidence suggests that EMT enhances tumor cell invasion in response to environmental triggers, augments invasive functions, and also contributes to cell growth and survival [14, 15]. In preliminary experiments, we found that upregulated UTR1 expression in metastatic CRC cell lines predicted poor survival for CRC patients. This current study was designed to search the evidence supporting a role for TUG1 in the metastasis of CRC in representative CRC cell lines. We further attempted the preliminary exploration of the possible association of EMT-related gene expression by TUG1.patients who had undergone gastrointestinal surgery between 2008 and 2013 at t.