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      Long noncoding RNA DANCR promotes colorectal cancer proliferation and metastasis via miR-577 sponging

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          Abstract

          Long non-coding RNAs (lncRNAs) play key roles in various malignant tumors, including colorectal cancer (CRC). Long non-coding RNA differentiation antagonizing non-protein coding RNA (DANCR) is overexpressed in CRC patients, but whether it affects CRC proliferation and metastasis via regulation of heat shock protein 27 (HSP27) remains unclear. In the present study, we found that DANCR was highly expressed and correlated with proliferation and metastasis in CRC. In addition, we demonstrated that DANCR and HSP27 were both targets of microRNA-577 (miR-577) and shared the same binding site. Furthermore, we revealed that DANCR promoted HSP27 expression and its mediation of proliferation/metastasis via miR-577 sponging. Finally, using an in vivo study, we confirmed that overexpression of DANCR promoted CRC tumor growth and liver metastasis. The present study demonstrated the function of DANCR in CRC and might provide a new target in the treatment of CRC.

          Colorectal cancer: Long non-coding RNA offers new drug target

          A long non-coding RNA linked to colorectal cancer causes tumor progression by unleashing the activity of a protein involved in cell proliferation and spread. Researchers in China led by Xiandong Zeng from Shenyang Medical College explain why the expression of a long non-coding RNA molecule known as DANCR correlates with poor prognosis in patients and mouse models carrying colorectal cancer tissue. They showed that DANCR displaces a small regulatory microRNA from its normal binding spot on the gene transcript that encodes HSP27, a protein involved in the growth and metastasis of colorectal cancer cells. This microRNA normally suppresses HSP27 activity, whereas DANCR, by outcompeting the microRNA, promotes HSP27 expression, leading to cell proliferation and metastasis. Drugs that block DANCR could thus help treat the disease.

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          Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma

          Mengge Huang, Zhenyu Zhong, Mengxin Lv … (2016)
          Accumulating evidences indicate that long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs) play important roles in tumorigenesis. However, the mechanisms remain largely unknown. To explore lncRNAs and circRNAs expression profiling and their biological functions in bladder cancer, we surveyed the lncRNA/circRNA and mRNA expression profiles of bladder cancer and para-cancer tissues using microarray for four patients. Thousands of significantly changed lncRNAs and mRNAs as well as hundreds of circRNAs were identified. Five dysregulated lncRNAs and four mRNAs were confirmed by quantitative real-time PCR in 30 pairs of samples. GO and KEGG pathway enrichment analyses were executed to determine the principal functions of the significantly deregulated genes. Further more, we constructed correlated expression networks including coding-noncoding co-expression (CNC), competing endogenous RNAs (ceRNA), cis regulation, lncRNAs-transcription factor (TF)-mRNA with bioinformatics methods. Co-expression analysis showed lncRNA APLP2 expression is correlated with apoptosis-related genes, including PTEN and TP53INP1. CeRNA network inferred that lncRNA H19 and circRNA MYLK could bind competitively with miRNA-29a-3p increasing target gene DNMT3B, VEGFA and ITGB1 expressions. Moreover, the nearby genes pattern displayed that overexpressing ADAM2 and C8orf4 are cis-regulated by lncRNA RP11-359E19.2, involving in progression of bladder cancer. In addition, lncRNAs-TF-mRNA diagram indicated that lncRNA BC041488 could trans-regulate CDK1 mRNA expression through SRF transcription factor. Taken together, these results suggested lncRNAs and circRNAs could implicate in the pathogenesis and development of bladder cancer. Our findings provide a novel perspective on lncRNAs and circRNAs and lay the foundation for future research of potential roles of lncRNAs and circRNAs in bladder carcinoma.
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            Competing endogenous RNA networks and gastric cancer.

            Lei-Lei Guo, Chun-Hua Song, Peng Wang … (2015)
            Recent studies have showed that RNAs regulate each other with microRNA (miRNA) response elements (MREs) and this mechanism is known as "competing endogenous RNA (ceRNA)" hypothesis. Long non-coding RNAs (lncRNAs) are supposed to play important roles in cancer. Compelling evidence suggests that lncRNAs can interact with miRNAs and regulate the expression of miRNAs as ceRNAs. Several lncRNAs such as H19, HOTAIR and MEG3 have been found to be associated with miRNAs in gastric cancer (GC), generating regulatory crosstalk across the transcriptome. These MRE sharing elements implicated in the ceRNA networks (ceRNETs) are able to regulate mRNA expression. The ceRNA regulatory networks including mRNAs, miRNAs, lncRNAs and circular RNAs may play critical roles in tumorigenesis, and the perturbations of ceRNETs may contribute to the pathogenesis of GC.
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              Hsp27 regulates epithelial mesenchymal transition, metastasis, and circulating tumor cells in prostate cancer.

              Eliana Beraldi, Martin Gleave, Jenny Bazov … (2013)
              Defining the mechanisms underlying metastatic progression of prostate cancer may lead to insights into how to decrease morbidity and mortality in this disease. An important determinant of metastasis is epithelial-to-mesenchymal transition (EMT), and the mechanisms that control the process of EMT in cancer cells are still emerging. Here, we report that the molecular chaperone Hsp27 (HSPB1) drives EMT in prostate cancer, whereas its attenuation reverses EMT and decreases cell migration, invasion, and matrix metalloproteinase activity. Mechanistically, silencing Hsp27 decreased IL-6-dependent STAT3 phosphorylation, nuclear translocation, and STAT3 binding to the Twist promoter, suggesting that Hsp27 is required for IL-6-mediated EMT via modulation of STAT3/Twist signaling. We observed a correlation between Hsp27 and Twist in patients with prostate cancer, with Hsp27 and Twist expression each elevated in high-grade prostate cancer tumors. Hsp27 inhibition by OGX-427, an antisense therapy currently in phase II trials, reduced tumor metastasis in a murine model of prostate cancer. More importantly, OGX-427 treatment decreased the number of circulating tumor cells in patients with metastatic castration-resistant prostate cancer in a phase I clinical trial. Overall, this study defines Hsp27 as a critical regulator of IL-6-dependent and IL-6-independent EMT, validating this chaperone as a therapeutic target to treat metastatic prostate cancer. ©2013 AACR.
              Article 0 comments Cited 79 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Xiandong Zeng:
                ORCID: http://orcid.org/0000-0003-0593-4147
                +86-24-85715888 , ZXD_landy1116@163.com
                Journal
                Journal ID (nlm-ta): Exp Mol Med
                Journal ID (iso-abbrev): Exp. Mol. Med
                Title: Experimental & Molecular Medicine
                Publisher: Nature Publishing Group UK (London )
                ISSN (Print): 1226-3613
                ISSN (Electronic): 2092-6413
                Publication date (Electronic): 1 May 2018
                Publication date PMC-release: 1 May 2018
                Publication date Collection: May 2018
                Volume: 50
                Issue: 5
                Electronic Location Identifier: 57
                Affiliations
                [1 ]GRID grid.459424.a, The 4th Department of Orthopedic Surgery, , Central Hospital Affiliated to Shenyang Medical College, ; Shenyang, 110024 China
                [2 ]GRID grid.452435.1, Department of Nuclear Medicine, , The First Affiliated Hospital of Dalian Medical University, ; Dalian, 116011 China
                [3 ]GRID grid.459424.a, The 2nd Department of Cardiology, , Central Hospital Affiliated to Shenyang Medical College, ; Shenyang, 110024 China
                [4 ]GRID grid.459424.a, Department of Pathology, , Central Hospital Affiliated to Shenyang Medical College, ; Shenyang, 110024 China
                [5 ]GRID grid.459424.a, Department of Surgical Oncology, , Central Hospital Affiliated to Shenyang Medical College, ; Shenyang, 110024 China
                Author information
                http://orcid.org/0000-0003-0593-4147
                Article
                Publisher ID: 82
                DOI: 10.1038/s12276-018-0082-5
                PMC ID: 5938019
                PubMed ID: 29717105
                SO-VID: bde02c35-e361-4a59-ad77-1b5cd14a6c8f
                Copyright © © The Author(s) 2018
                License:

                Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, and provide a link to the Creative Commons license. You do not have permission under this license to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, http://creativecommons.org/licenses/by-nc-nd/4.0/.

                History
                Date received : 31 October 2017
                Date revision received : 23 January 2018
                Date accepted : 14 February 2018
                Categories
                Subject: Article
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                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Molecular medicine
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                ScienceOpen disciplines: Molecular medicine

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