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      Resveratrol Inhibits Invasion and Metastasis of Colorectal Cancer Cells via MALAT1 Mediated Wnt/β-Catenin Signal Pathway

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          Abstract

          Resveratrol, extracted from Chinese herbal medicine Polygonum cuspidatum, is known to inhibit invasion and metastasis of human colorectal cancer (CRC), in which long non-coding Metastasis Associated Lung Adenocarcinoma Transcript 1 (RNA-MALAT1) also plays an important role. Using MALAT1 lentiviral shRNA and over-expression constructs in CRC derived cell lines, LoVo and HCT116, we demonstrated that the anti-tumor effects of resveratrol on CRC are through inhibiting Wnt/β-catenin signaling, thus the expression of its target genes such as c-Myc, MMP-7, as well as the expression of MALAT1. In detail, resveratrol down-regulates MALAT1, resulting in decreased nuclear localization of β-catenin thus attenuated Wnt/β-catenin signaling, which leads to the inhibition of CRC invasion and metastasis. This finding of ours surely provides important pre-clinical evidence supporting future use of resveratrol in prevention and treatment of CRC.

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          MALAT-1: a long non-coding RNA and its important 3' end functional motif in colorectal cancer metastasis.

          Minhui Yang, Xiaoyan Wang, Zuguo Li … (2011)
          The human metastasis associated lung adenocarcinoma transcript 1 (MALAT-1) as a long non-coding RNA known to be misregulated in many people who are detected with cancer. Our earlier studies found that MALAT-1 plays a pivotal role in colorectal cancer (CRC) metastasis. In this study, we analyzed the MALAT-1 gene in five fragments. We employed the sequencing process to identify MALAT-1 mutations in the following types of samples: CRC cells (SW620, SW480), normal colorectal tissues, and primary CRC tissues. We were successful in detecting the following mutations: fragment 5434 nt-6951 nt of the MALAT-1 was mutated in SW620 cells, while fragments 5434 nt-6951 nt and 6918 nt-8441 nt of MALAT-1 were mutated in SW480 cancer cells and primary CRC tissues. We over-expressed five fragments of MALAT-1 in the CRC cell line SW480; simultaneously ensuring that MALAT-1 had low expression. Our data illustrated that one of the 5 fragments (6918 nt-8441 nt) located at the 3' end of MALAT-1 plays a pivotal role in the biological processes of cell proliferation, migration and invasion. Based on these observations, we can infer that the 3' end of MALAT-1 is an important biological motif in the invasion and metastasis of CRC cells. We have successfully presented the first evidence that mutations were found on the long non-coding RNA MALAT-1 in CRC. Moreover, long non-coding RNA MALAT-1 has an important biological motif located at the 3' end of MALAT-1 (6918 nt-8441 nt) in CRC. Our study gives a new direction to research primarily focused on exploring the molecular mechanisms occurring during the invasion and metastasis of CRC.
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            Resveratrol induces apoptosis and inhibits angiogenesis in human breast cancer xenografts in vivo.

            Stina Garvin, Karin Öllinger, Charlotta Dabrosin (2006)
            Resveratrol, a polyphenol found in grapes and wine, is considered a potential cancer chemopreventive agent. Resveratrol has been shown to induce transcription via both ERalpha and ERbeta. We observed significantly lower tumor growth, decreased angiogenesis, and increased apoptotic index in ERalpha- ERbeta+ MDA-MB-231 tumors in resveratrol-treated nude mice compared with controls. In vitro we found a significant increase in apoptosis in resveratrol-treated MDA-MB-231 cells in addition to significantly reduced extracellular levels of VEGF. This study supports the potential use of resveratrol as a chemotherapeutic agent in breast cancers.
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              A vital role for Ape1/Ref1 protein in repairing spontaneous DNA damage in human cells.

              Jeffrey W H Fung, Bruce Demple (2005)
              Discovered as a DNA repair protein, Ape1 has been associated with other functions, notably redox regulation of transcription factors (Ref1 activity). Because deletion of the mouse gene produces embryonic lethality and stable Ape1-deficient cell lines have not been reported, there has been uncertainty about a possible vital cellular function of Ape1. We addressed this issue by using RNA interference (RNAi) in several human cell types. Strong downregulation of Ape1 stopped cell proliferation and activated apoptosis, which was correlated with accumulation of abasic DNA damage. These effects were reversed by expression of yeast Apn1 protein, which is structurally unrelated to Ape1 but shares enzymatic activity in repair of abasic sites (AP endonuclease). Because Apn1 would lack Ref1 activity or the protein interactions of Ape1, we conclude that the AP endonuclease activity is essential for cellular viability. Accumulation of abasic DNA damage from intrinsic sources appears sufficient to trigger cell death when Ape1-mediated repair is deficient.
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                Author and article information

                Contributors
                Irina U. Agoulnik: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, USA )
                ISSN (Electronic): 1932-6203
                Publication date Collection: 2013
                Publication date (Electronic): 11 November 2013
                Volume: 8
                Issue: 11
                Electronic Location Identifier: e78700
                Affiliations
                [1 ]Department of Medical Oncology, Shuguang Hospital; Shanghai University of Traditional Chinese Medicine, Shanghai, China
                [2 ]Interventional Cancer Institute & Department of General Surgery, Shanghai University of Traditional Chinese Medicine, Shanghai, China
                [3 ]Department of Chemistry, University of South Florida, Tampa, Florida, United States of America
                [4 ]Department of Oncology, Shanghai Municipal Hospital of Traditional Chinese Medicine, S, hanghai, China
                Florida International University, United States of America
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Conceived and designed the experiments: JR QL. Performed the experiments: QJ XL HS LZ(Long Zhang) YW JS. Analyzed the data: QJ XF HZ JC JQ QL LZ(Lihong Zhou). Contributed reagents/materials/analysis tools: QJ JC QL. Wrote the manuscript: QJ JR QL.

                Article
                Publisher ID: PONE-D-13-19038
                DOI: 10.1371/journal.pone.0078700
                PMC ID: 3823921
                PubMed ID: 24244343
                SO-VID: c21622bb-e501-4883-afea-7d9c7330b743
                Copyright statement: Copyright @ 2013
                License:

                This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.

                History
                Date received : 9 May 2013
                Date accepted : 15 September 2013
                Page count
                Pages: 12
                Funding
                This work was supported by National Natural Science Foundation of China (81202812, 81303102, 81303103), Program of Shanghai Municipal Education Commission (2011JW57, 12YZ058), Shanghai Municipal Health Bureau (ZYSNXD-CC-YJXYY-JS20, 2011ZJ030, 20114Y001, 20114037), Shanghai Key Laboratory of Traditional Chinese Clinical Medicine (C10dz2220200). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Uncategorized
                Data availability:
                ScienceOpen disciplines: Uncategorized

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