The multiple roles of microRNA-155 in oncogenesis

Journal of Clinical Bioinformatics

Frank Slack¹  Gadareth Higgs² 

[1] Department of Molecular, Cellular and Developmental Biology, Yale University, KBT 936, PO Box 208103, New Haven, CT 06520, USA;Yale Center for Medical Informatics, Yale University, Suite 505, 300 George Street, New Haven, USA

关键词: Nanoparticle delivery;    Anti-miR therapy;    OncomiRs;    Oncogenesis;    miR-155;   

Others  :  801581
DOI  :  10.1186/2043-9113-3-17

 received in 2013-07-22, accepted in 2013-09-25,  发布年份 2013

【 摘 要 】

The microRNA miR-155 is prominent in cancer biology. Among microRNAs that have been linked to cancer, it is the most commonly overexpressed in malignancies (PNAS 109:20047-20052, 2012). Since its discovery, miR-155 has been implicated in promoting cancers of the breast, lung, liver, and lymphatic system. As such, targeted therapies may prove beneficial to cancer treatment. This review discusses the important role of miR-155 in oncogenesis. It synthesizes information from ten recent papers on miR-155, and includes an analysis and discussion of its association with cancer, interactions with other miRNAs, mechanisms of action, and the most promising available treatment options.

Current debates in the field include the importance of miRNAs in general and their utility as targets in preventing tumorigenesis (Blood 119:513-520, 2012). Most of the papers being reviewed here confirm the role of miR-155 in oncogenesis (EMBO Mol Med 1:288-295, 2009). While there is some controversy surrounding recent research that claims that miR-155 may display anti-oncogenic or pro-immunological benefits (Cell Rep 2:1697–1709, 2012), most research seems to point to the importance of anti-miRs, with anti-miR-155 in particular, for cancer therapy.

【 授权许可】

   
2013 Higgs and Slack; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

Figure 2.

【 参考文献 】

• [1]Bartel DP: MicroRNAs: target recognition and regulatory functions. Cell 2009, 136(2):215-233.
• [2]Filipowicz W, Bhattacharyya SN, Sonenberg N: Mechanisms of post-transcriptional regulation by microRNAs: are the answers in sight? Nat Rev Genet 2008, 9(2):102-114.
• [3]Zhang P, Bill K, Liu J, Young E, Peng T, Bolshakov S, Hoffman A, Song Y, Demicco EG, Terrada DL, et al.: MiR-155 is a liposarcoma oncogene that targets casein kinase-1alpha and enhances beta-catenin signaling. Cancer Res 2012, 72(7):1751-1762.
• [4]Faraoni I, Antonetti FR, Cardone J, Bonmassar E: miR-155 gene: a typical multifunctional microRNA. Biochimica et biophysica acta 2009, 1792(6):497-505.
• [5]Stahlhut Espinosa CE, Slack FJ: The role of microRNAs in cancer. Yale J Biol Med 2006, 79(3–4):131-140.
• [6]Kala R, Peek GW, Hardy TM, Tollefsbol TO: MicroRNAs: an emerging science in cancer epigenetics. J Clin Bioinform 2013, 3(1):6. BioMed Central Full Text
• [7]Teng G, Papavasiliou FN: Shhh! Silencing by microRNA-155. Philos Transac Royal Soc Lond Series B 2009, 364(1517):631-637.
• [8]Sandhu SK, Volinia S, Costinean S, Galasso M, Neinast R, Santhanam R, Parthun MR, Perrotti D, Marcucci G, Garzon R, et al.: miR-155 targets histone deacetylase 4 (HDAC4) and impairs transcriptional activity of B-cell lymphoma 6 (BCL6) in the Emu-miR-155 transgenic mouse model. Proc Nat Acad Sci USA 2012, 109(49):20047-20052.
• [9]Tili E, Michaille JJ, Adair B, Alder H, Limagne E, Taccioli C, Ferracin M, Delmas D, Latruffe N, Croce CM: Resveratrol decreases the levels of miR-155 by upregulating miR-663, a microRNA targeting JunB and JunD. Carcinogen 2010, 31(9):1561-1566.
• [10]Donnem T, Eklo K, Berg T, Sorbye SW, Lonvik K, Al-Saad S, Al-Shibli K, Andersen S, Stenvold H, Bremnes RM, et al.: Prognostic impact of MiR-155 in non-small cell lung cancer evaluated by in situ hybridization. J Trans Med 2011, 9:6. BioMed Central Full Text
• [11]Tili E, Croce CM, Michaille JJ: miR-155: on the crosstalk between inflammation and cancer. Int Rev Immunol 2009, 28(5):264-284.
• [12]Calame K: MicroRNA-155 function in B Cells. Immunity 2007, 27(6):825-827.
• [13]Thai TH, Calado DP, Casola S, Ansel KM, Xiao C, Xue Y, Murphy A, Frendewey D, Valenzuela D, Kutok JL, et al.: Regulation of the germinal center response by microRNA-155. Science 2007, 316(5824):604-608.
• [14]Dagan LN, Jiang X, Bhatt S, Cubedo E, Rajewsky K, Lossos IS: miR-155 regulates HGAL expression and increases lymphoma cell motility. Blood 2012, 119(2):513-520.
• [15]Babar IA, Cheng CJ, Booth CJ, Liang X, Weidhaas JB, Saltzman WM, Slack FJ: Nanoparticle-based therapy in an in vivo microRNA-155 (miR-155)-dependent mouse model of lymphoma. Proc Nat Acad Sci USA 2012, 109(26):E1695-E1704.
• [16]Jiang S, Zhang LF, Zhang HW, Hu S, Lu MH, Liang S, Li B, Li Y, Li D, Wang ED, et al.: A novel miR-155/miR-143 cascade controls glycolysis by regulating hexokinase 2 in breast cancer cells. EMBO J 2012, 31(8):1985-1998.
• [17]Li S, Chen T, Zhong Z, Wang Y, Li Y, Zhao X: microRNA-155 silencing inhibits proliferation and migration and induces apoptosis by upregulating BACH1 in renal cancer cells. Mol Med Rep 2012, 5(4):949-954.
• [18]Forrest AR, Kanamori-Katayama M, Tomaru Y, Lassmann T, Ninomiya N, Takahashi Y, de Hoon MJ, Kubosaki A, Kaiho A, Suzuki M, et al.: Induction of microRNAs, mir-155, mir-222, mir-424 and mir-503, promotes monocytic differentiation through combinatorial regulation. Leukemia 2010, 24(2):460-466.
• [19]Willimott S, Wagner SD: miR-125b and miR-155 contribute to BCL2 repression and proliferation in response to CD40 ligand (CD154) in human leukemic B-cells. J Biol Chem 2012, 287(4):2608-2617.
• [20]Chang S, Wang RH, Akagi K, Kim KA, Martin BK, Cavallone L, Haines DC, Basik M, Mai P, Kathleen Cuningham Foundation Consortium for Research into Familial Breast C, et al.: Tumor suppressor BRCA1 epigenetically controls oncogenic microRNA-155. Nature Med 2011, 17(10):1275-1282.
• [21]Pedersen IM, Otero D, Kao E, Miletic AV, Hother C, Ralfkiaer E, Rickert RC, Gronbaek K, David M: Onco-miR-155 targets SHIP1 to promote TNFalpha-dependent growth of B cell lymphomas. EMBO Mol Med 2009, 1(5):288-295.
• [22]Linnstaedt SD, Gottwein E, Skalsky RL, Luftig MA, Cullen BR: Virally induced cellular microRNA miR-155 plays a key role in B-cell immortalization by Epstein-Barr virus. J Virol 2010, 84(22):11670-11678.
• [23]Huffaker TB, Hu R, Runtsch MC, Bake E, Chen X, Zhao J, Round JL, Baltimore D, O’Connell RM: Epistasis between microRNAs 155 and 146a during T cell-mediated antitumor immunity. Cell Rep 2012, 2(6):1697-1709.
• [24]Zonari E, Pucci F, Saini M, Mazzieri R, Politi LS, Gentner B, Naldini L: A role for miR-155 in enabling tumor-infiltrating innate immune cells to mount effective anti-tumor responses. Blood 2013, 122(2):243-252.
• [25]Meeran SM, Ahmed A, Tollefsbol TO: Epigenetic targets of bioactive dietary components for cancer prevention and therapy. Clin Epigenet 2010, 1(3–4):101-116.
• [26]Hardy TM, Tollefsbol TO: Epigenetic diet: impact on the epigenome and cancer. Epigenom 2011, 3(4):503-518.
• [27]Landis-Piwowar KR, Huo C, Chen D, Milacic V, Shi G, Chan TH, Dou QP: A novel prodrug of the green tea polyphenol (−)-epigallocatechin-3-gallate as a potential anticancer agent. Cancer Res 2007, 67(9):4303-4310.
• [28]Zhang M, Zhou X, Wang B, Yung BC, Lee LJ, Ghoshal K, Lee RJ: Lactosylated gramicidin-based lipid nanoparticles (Lac-GLN) for targeted delivery of anti-miR-155 to hepatocellular carcinoma. J Cont Release 2013, 168(3):251-261.
• [29]Vigorito E, Kohlhaas S, Lu D, Leyland R: miR-155: an ancient regulator of the immune system. Immunolog Rev 2013, 253(1):146-157.
• [30]Li Y, Liu L, Tollefsbol TO: Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression. FASEB J 2010, 24(5):1442-1453.
• [31]Hanahan D, Weinberg RA: Hallmarks of cancer: the next generation. Cell 2011, 144(5):646-674.
• [32]Schetter AJ, Heegaard NH, Harris CC: Inflammation and cancer: interweaving microRNA, free radical, cytokine and p53 pathways. Carcinogen 2010, 31(1):37-49.
• [33]Hussain SP, Harris CC: Inflammation and cancer: an ancient link with novel potentials. Int J Cancer 2007, 121(11):2373-2380.