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      miR-146b promotes cell proliferation and increases chemosensitivity, but attenuates cell migration and invasion via FBXL10 in ovarian cancer

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          Abstract

          Epithelial ovarian carcinoma (EOC) is the most lethal gynecologic malignancy. However, the molecular mechanisms remain unclear. In this study, we found that miR-146b was downregulated in EOC and its expression level was negatively correlated with the pathological staging. Follow-up functional experiments illustrated that overexpression of miR-146b significantly inhibited cell migration and invasion, and increased cell proliferation, but it also improved the response to chemotherapeutic agents. Mechanistically, we demonstrated that miR-146b exerted its function mainly through inhibiting F-box and leucine-rich repeat protein 10 (FBXL10), and upregulated the Cyclin D1, vimentin (VIM), and zona-occludens-1 (ZO-1) expression in EOC. These findings indicate that miR-146b–FBXL10 axis is an important epigenetic regulation pathway in EOC. Low miR-146b may contribute to cancer progression from primary stage to advanced stage, and may be the promising therapeutic target of EOC.

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          miR-141 and miR-200a act on ovarian tumorigenesis by controlling oxidative stress response.

          Bogdan Mateescu, Luciana Moreira Batista, Melissa Cardon … (2011)
          Although there is evidence that redox regulation has an essential role in malignancies, its impact on tumor prognosis remains unclear. Here we show crosstalk between oxidative stress and the miR-200 family of microRNAs that affects tumorigenesis and chemosensitivity. miR-141 and miR-200a target p38α and modulate the oxidative stress response. Enhanced expression of these microRNAs mimics p38α deficiency and increases tumor growth in mouse models, but it also improves the response to chemotherapeutic agents. High-grade human ovarian adenocarcinomas that accumulate miR-200a have low concentrations of p38α and an associated oxidative stress signature. The miR200a-dependent stress signature correlates with improved survival of patients in response to treatment. Therefore, the role of miR-200a in stress could be a predictive marker for clinical outcome in ovarian cancer. In addition, although oxidative stress promotes tumor growth, it also sensitizes tumors to treatment, which could account for the limited success of antioxidants in clinical trials.
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            Expression of microRNA-146 suppresses NF-kappaB activity with reduction of metastatic potential in breast cancer cells.

            D Bhaumik, G. Scott, S Schokrpur … (2008)
            Cancer cells often acquire a constitutively active nuclear factor-kappaB (NF-kappaB) program to promote survival, proliferation and metastatic potential by mechanisms that remain largely unknown. Extending observations from an immunologic setting, we demonstrate that microRNA-146a and microRNA-146b (miR-146a/b) when expressed in the highly metastatic human breast cancer cell line MDA-MB-231 function to negatively regulate NF-kappaB activity. Lentiviral-mediated expression of miR-146a/b significantly downregulated interleukin (IL)-1 receptor-associated kinase and TNF receptor-associated factor 6, two key adaptor/scaffold proteins in the IL-1 and Toll-like receptor signaling pathway, known to positively regulate NF-kappaB activity. Impaired NF-kappaB activity was evident from reduced phosphorylation of the NF-kappaB inhibitor IkappaBalpha, reduced NF-kappaB DNA-binding activity and suppressed expression of the NF-kappaB target genes IL-8, IL-6 and matrix metalloproteinase-9. Functionally, miR-146a/b-expressing MDA-MB-231 cells showed markedly impaired invasion and migration capacity relative to control cells. These findings implicate miR-146a/b as a negative regulator of constitutive NF-kappaB activity in a breast cancer setting and suggest that modulating miR-146a/b levels has therapeutic potential to suppress breast cancer metastases.
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              Contextual extracellular cues promote tumor cell EMT and metastasis by regulating miR-200 family expression.

              Don L. Gibbons, Wei Lin, Chad J. Creighton … (2009)
              Metastatic disease is a primary cause of cancer-related death, and factors governing tumor cell metastasis have not been fully elucidated. Here, we address this question by using tumor cell lines derived from mice that develop metastatic lung adenocarcinoma owing to expression of mutant K-ras and p53. Despite having widespread somatic genetic alterations, the metastasis-prone tumor cells retained a marked plasticity. They transited reversibly between epithelial and mesenchymal states, forming highly polarized epithelial spheres in three-dimensional culture that underwent epithelial-to-mesenchymal transition (EMT) following treatment with transforming growth factor-beta or injection into syngeneic mice. This transition was entirely dependent on the microRNA (miR)-200 family, which decreased during EMT. Forced expression of miR-200 abrogated the capacity of these tumor cells to undergo EMT, invade, and metastasize, and conferred transcriptional features of metastasis-incompetent tumor cells. We conclude that tumor cell metastasis is regulated by miR-200 expression, which changes in response to contextual extracellular cues.
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                Author and article information

                Contributors
                Qixiang Shao:
                ORCID: http://orcid.org/0000-0002-8332-1605
                +86-0511-85038145 , shao_qx@ujs.edu.cn
                Journal
                Journal ID (nlm-ta): Cell Death Dis
                Journal ID (iso-abbrev): Cell Death Dis
                Title: Cell Death & Disease
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2041-4889
                Publication date (Electronic): 8 November 2018
                Publication date PMC-release: 8 November 2018
                Publication date Collection: November 2018
                Volume: 9
                Issue: 11
                Electronic Location Identifier: 1123
                Affiliations
                [1 ]ISNI 0000 0001 0743 511X, GRID grid.440785.a, Department of Immunology, Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, , Jiangsu University, ; Zhenjiang, 212013 Jiangsu China
                [2 ]ISNI 0000 0004 1799 0784, GRID grid.412676.0, Department of Pathology, Nanjing Drum Tower Hospital, , The Affiliated Hospital of Nanjing University Medical School, ; Nanjing, 210008 Jiangsu China
                [3 ]GRID grid.452247.2, Department of Gynecology and Obstetrics, , Affiliated Hospital of Jiangsu University, ; Zhenjiang, 212001 Jiangsu China
                [4 ]GRID grid.452247.2, Department of Pathology, , Affiliated People’s Hospital of Jiangsu University, ; Zhenjiang, 212001 Jiangsu China
                [5 ]GRID grid.452247.2, Department of ICU, , Affiliated Hospital of Jiangsu University, ; Zhenjiang, 212001 Jiangsu China
                [6 ]Department of Wuxi Maternal and Child Health Care Hospital, Wuxi, 214000 Jiangsu China
                Author information
                http://orcid.org/0000-0002-8332-1605
                Article
                Publisher ID: 1093
                DOI: 10.1038/s41419-018-1093-9
                PMC ID: 6224598
                PubMed ID: 30409964
                SO-VID: 639efe17-9484-4cb5-8d07-d272d0aad95a
                Copyright © © The Author(s) 2018
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 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, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 29 May 2018
                Date revision received : 24 August 2018
                Date accepted : 10 September 2018
                Funding
                Funded by: 1 Clinical Medicine Science & Technology Project of Jiangsu province of China (Grant No. BL2013024) 2 Chinese National Natural Science Foundation Grant (Grant No. 81273202, 81671541, 31400773) 3 Key research and development Programs social development project of Science and Technology Commission Foundation of Jiangsu Province (Grant No. BE2016604, BE2016721)
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Cell biology
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                ScienceOpen disciplines: Cell biology

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