For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
12
views
18
references
 Top references
cited by
15
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      415
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Long non-coding RNA NNT-AS1 functions as an oncogenic gene through modulating miR-485/BCL9 in cholangiocarcinoma

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Introduction

          Growing evidence suggests that long non-coding RNAs (lncRNAs) could function as important regulators in carcinogenesis and cancer progression. Nicotinamide nucleotide transhydrogenase antisense RNA 1 (lncRNA NNT-AS1) is up-regulated in some human tumors and functions as a tumor promoter. This study aimed to detect the effect of NNT-AS1 on cholangiocarcinoma (CCA) prognosis.

          Materials and methods

          In this study, we detected NNT-AS1 expression in CCA tissue samples and cell lines, and analyzed the association between NNT-AS1 expression levels and clinical parameters of CCA patients. Moreover, we conducted loss-of-function studies in CCA cancer cells to explore the biological function and molecular mechanism of NNT-AS1. NNT-AS1 was downregulated by using RNAi technology. Cell proliferation was examined by CCK8 and clone formation assays. Cell migration and invasion were determined by wound healing and transwell assays. Western blot assays were used to explore protein expression.

          Results

          In this study, NNT-AS1 was expressed at high levels in CCA and closely associated with poor prognosis of patients with CCA. NNT-AS1 knockdown impaired cell proliferation, suppressed CCA cell migration and invasion, and restrained tumor growth in vitro. Moreover, NNT-AS1 directly bounded to miR-485 and further regulated BCL9. Finally, rescue assays verified that NNT-AS1 modulated the tumorigenesis of CCA by regulating miR-485.

          Conclusion

          Taken together, NNT-AS1 played a critical biological role in the development of CCA. Our results elucidated NNT-AS1/miR-485/BCL9 axis might lead to a further understanding of the molecular mechanism of CCA.

          Related collections

          Most cited references18

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          Cholangiocarcinoma: Current Knowledge and New Developments

          Boris Blechacz (2016)
          Cholangiocarcinoma (CCA) is the second most common primary malignancy. Although it is more common in Asia, its incidence in Europe and North America has significantly increased in recent decades. The prognosis of CCA is dismal. Surgery is the only potentially curative treatment, but the majority of patients present with advanced stage disease, and recurrence after resection is common. Over the last two decades, our understanding of the molecular biology of this malignancy has increased tremendously, diagnostic techniques have evolved, and novel therapeutic approaches have been established. This review discusses the changing epidemiologic trends and provides an overview of newly identified etiologic risk factors for CCA. Furthermore, the molecular pathogenesis is discussed as well as the influence of etiology and biliary location on the mutational landscape of CCA. This review provides an overview of the diagnostic evaluation of CCA and its staging systems. Finally, new therapeutic options are critically reviewed, and future therapeutic strategies discussed.
          Article 0 comments Cited 177 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Targeted disruption of the BCL9/β-catenin complex inhibits oncogenic Wnt signaling.

            Kohichi Takada, Di Zhu, Gregory Bird … (2012)
            Deregulated Wnt/β-catenin signaling underlies the pathogenesis of a broad range of human cancers, yet the development of targeted therapies to disrupt the resulting aberrant transcription has proved difficult because the pathway comprises large protein interaction surfaces and regulates many homeostatic functions. Therefore, we have directed our efforts toward blocking the interaction of β-catenin with B cell lymphoma 9 (BCL9), a co-activator for β-catenin-mediated transcription that is highly expressed in tumors but not in the cells of origin. BCL9 drives β-catenin signaling through direct binding mediated by its α-helical homology domain 2. We developed a stabilized α helix of BCL9 (SAH-BCL9), which we show targets β-catenin, dissociates native β-catenin/BCL9 complexes, selectively suppresses Wnt transcription, and exhibits mechanism-based antitumor effects. SAH-BCL9 also suppresses tumor growth, angiogenesis, invasion, and metastasis in mouse xenograft models of Colo320 colorectal carcinoma and INA-6 multiple myeloma. By inhibiting the BCL9-β-catenin interaction and selectively suppressing oncogenic Wnt transcription, SAH-BCL9 may serve as a prototype therapeutic agent for cancers driven by deregulated Wnt signaling.
            Article 0 comments Cited 85 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Long non-coding RNA NNT-AS1 affects progression of breast cancer through miR-142-3p/ZEB1 axis

              Yan. Li, Zhi Lou, Ran Wang … (2018)
              Some evidences have been provided to verify the effects of lncRNA NNT-AS1 on cancer progression. However, the crucial impacts of NNT-AS1 on the malignancy of breast cancer have not been elaborated. This study aims to detect the expression pattern and functional effects of NNT-AS1 in breast cancer. qRT-PCR analysis was applied to detect the expression of NNT-AS1 in both BC tissues and matched normal tissues. Loss of function assay was carried out to detect the effects of silenced NNT-AS1 on proliferation, metastasis and EMT process of BC cells. To understand the functional mechanism of NNT-AS1, mechanism assays were designed and performed in BC cells. Subcellular fractionation assay demonstrated that NNT-AS1 was located in the cytoplasm of BC cells. Therefore, NNT-AS1 might exert ceRNA functions in BC cells. To validate this hypothesis, we found the combination between NNT-AS1 and miR-142-3p through conducting bioinformatics analysis, RIP and luciferase reporter assays. Similarly, the combination between miR-142-3p and ZEB1 was verified. Finally, the recue assays were carried out to demonstrate the effects of NNT-AS1/miR-142-3p/ZEB1 axis on the biological behaviors of BC cells. All the above findings revealed a fact that NNT-AS1 affects breast cancer progression through modulating miR-142-3p/ZEB1 axis.
              Article 0 comments Cited 42 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Cancer Manag Res
                Journal ID (iso-abbrev): Cancer Manag Res
                Journal ID (publisher-id): CMAR
                Journal ID (pmc): cancmanres
                Title: Cancer Management and Research
                Publisher: Dove
                ISSN (Electronic): 1179-1322
                Publication date (Electronic): 15 August 2019
                Publication date Collection: 2019
                Volume: 11
                Pages: 7739-7749
                Affiliations
                [1 ] Department of HPB Surgery, The 2nd Affiliated Hospital of Harbin Medical University , Harbin 150086, People’s Republic of China
                Author notes
                Correspondence: Yunfu CuiDepartment of HPB Surgery, The 2nd Affiliated Hospital of Harbin Medical University , 246 Xuefu-ro, Harbin150086, People’s Republic of ChinaTel +86 4 518 660 5043Email yfcui777@hotmail.com
                [*]

                These authors contributed equally to this work

                Author information
                http://orcid.org/0000-0003-1177-4530
                Article
                Publisher ID: 207801
                DOI: 10.2147/CMAR.S207801
                PMC ID: 6699498
                SO-VID: cd685c2c-dbac-4bf7-9534-aa344887e8a1
                Copyright © © 2019 Huang et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 12 March 2019
                Date accepted : 10 July 2019
                Page count
                Figures: 5, Tables: 1, References: 27, Pages: 11
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: lncrna,nnt-as1,cholangiocarcinoma,bcl9
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: lncrna, nnt-as1, cholangiocarcinoma, bcl9

                Comments

                Comment on this article

                scite_

                Similar content415

                See all similar

                Cited by15

                See all cited by

                Most referenced authors402

                See all reference authors