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      Suppressing miRNA-15a/-16 expression by interleukin-6 enhances drug-resistance in myeloma cells

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          Abstract

          The bone marrow microenvironment facilitates the survival, differentiation, and proliferation of myeloma (MM) cells. This study identified that microRNA-15a and -16 expressions tightly correlated with proliferation and drug sensitivity of MM cells. miRNA-15a/-16 expression in MM cells was significantly increased after treatment with cytotoxic agents. The interaction of bone marrow stromal cells (BMSC) with MM cells resulted in decreased miRNA-15a/-16 expression and promoted the survival of the MM cells. Interleukin-6 (IL-6) produced by BMSCs suppressed the expression of miRNA-15a and 16 in a time- and dose- dependent pattern, with the suppression on miRNA-15a being more significant than on miRNA-16. miRNA-15a-transfected MM cells were found to be arrested in G1/S checkpoint, and the transfected MM cells had decreased growth and survival. In conclusion, our data suggest that via suppressing miRNA-15a and -16 expressions, IL-6 secreted by BMSCs promotes drug-resistance in myeloma cells.

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          Novel histone deacetylase inhibitors in clinical trials as anti-cancer agents

          Jiahuai Tan, Shundong Cang, Yuehua Ma … (2010)
          Histone deacetylases (HDACs) can regulate expression of tumor suppressor genes and activities of transcriptional factors involved in both cancer initiation and progression through alteration of either DNA or the structural components of chromatin. Recently, the role of gene repression through modulation such as acetylation in cancer patients has been clinically validated with several inhibitors of HDACs. One of the HDAC inhibitors, vorinostat, has been approved by FDA for treating cutaneous T-cell lymphoma (CTCL) for patients with progressive, persistent, or recurrent disease on or following two systemic therapies. Other inhibitors, for example, FK228, PXD101, PCI-24781, ITF2357, MGCD0103, MS-275, valproic acid and LBH589 have also demonstrated therapeutic potential as monotherapy or combination with other anti-tumor drugs in CTCL and other malignancies. At least 80 clinical trials are underway, testing more than eleven different HDAC inhibitory agents including both hematological and solid malignancies. This review focuses on recent development in clinical trials testing HDAC inhibitors as anti-tumor agents.
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            Mechanism of action of lenalidomide in hematological malignancies

            Venumadhav Kotla, Swati Goel, Sangeeta Nischal … (2009)
            Immunomodulatory drugs lenalidomide and pomalidomide are synthetic compounds derived by modifying the chemical structure of thalidomide to improve its potency and reduce its side effects. Lenalidomide is a 4-amino-glutamyl analogue of thalidomide that lacks the neurologic side effects of sedation and neuropathy and has emerged as a drug with activity against various hematological and solid malignancies. It is approved by FDA for clinical use in myelodysplastic syndromes with deletion of chromosome 5q and multiple myeloma. Lenalidomide has been shown to be an immunomodulator, affecting both cellular and humoral limbs of the immune system. It has also been shown to have anti-angiogenic properties. Newer studies demonstrate its effects on signal transduction that can partly explain its selective efficacy in subsets of MDS. Even though the exact molecular targets of lenalidomide are not well known, its activity across a spectrum of neoplastic conditions highlights the possibility of multiple target sites of action.
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              Multiple myeloma: biology of the disease.

              Anuj Mahindra, K. Anderson, TERU HIDESHIMA (2010)
              Multiple myeloma (MM) is a clonal B-cell malignancy characterized by the aberrant expansion of plasma cells within the bone marrow, as well as at extramedullary sites. Decades of scientific research are now beginning to unravel the intricate biology that underlies the pathophysiology of MM. In particular, the roles of cellular differentiation, molecular pathogenesis, and oncogenes involved in the natural history of MM are becoming clearer. This has enabled the identification of specific cytokines, adhesion molecules, and stromal cells that affect MM cell development, disease progression, and treatment responses. This review describes our current understanding regarding the biology of MM, and how this has led to a robust pipeline of novel therapeutic agents with the potential to overcome resistance to existing MM therapies and, therefore, further improve outcomes in patients with MM. Copyright © 2010 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Hematol Oncol
                Title: Journal of Hematology & Oncology
                Publisher: BioMed Central
                ISSN (Electronic): 1756-8722
                Publication date Collection: 2011
                Publication date (Electronic): 22 September 2011
                Volume: 4
                Page: 37
                Affiliations
                [1 ]State Key Laboratory of Experimental Hematology, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Science & Peking Union Medical College Tianjin China
                [2 ]West China Hospital, Sichuan University. Blood Section, Chengdu, Sichuan, China
                [3 ]Department of Laboratory Hematology, University Health Network, University of Toronto, Canada
                Article
                Publisher ID: 1756-8722-4-37
                DOI: 10.1186/1756-8722-4-37
                PMC ID: 3189173
                PubMed ID: 21936961
                SO-VID: b5d2fdb8-47fa-4219-b715-700a05effc44
                Copyright © Copyright ©2011 Hao et al; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 24 August 2011
                Date accepted : 22 September 2011
                Categories
                Subject: Letter to the Editor

                ScienceOpen disciplines: Oncology & Radiotherapy
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy

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