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miRNAs and Melanoma: How Are They Connected?

DOI: 10.1155/2012/528345

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Abstract:

miRNAs are non-coding RNAs that bind to mRNA targets and disturb their stability and/or translation, thus acting in gene posttranscriptional regulation. It is predicted that over 30% of mRNAs are regulated by miRNAs. Therefore these molecules are considered essential in the processing of many biological responses, such as cell proliferation, apoptosis, and stress responsiveness. As miRNAs participate of virtually all cellular pathways, their deregulation is critical to cancer development. Consequently, loss or gain of miRNAs function may contribute to tumor progression. Little is known about the regulation of miRNAs and understanding the events that lead to changes in their expression may provide new perspectives for cancer treatment. Among distinct types of cancer, melanoma has special implications. It is characterized as a complex disease, originated from a malignant transformation of melanocytes. Despite being rare, its metastatic form is usually incurable, which makes melanoma the major death cause of all skin cancers. Some molecular pathways are frequently disrupted in melanoma, and miRNAs probably have a decisive role on these alterations. Therefore, this review aims to discuss new findings about miRNAs in melanoma fields, underlying epigenetic processes, and also to argue possibilities of using miRNAs in melanoma diagnosis and therapy. 1. Introduction Gene expression profiles characterize cells of specific tissues. Alterations on these patterns can promote cell homeostasis disruption leading to the appearance of some diseases, including cancer. In this regard, it is very important to comprehend how gene expression is regulated. One of the mechanisms of gene control is associated with the dynamic equilibrium between mRNA translation and its degradation and this process is intermediated by a special class of noncoding small RNAs. miRNAs (microRNAs), siRNAs (small interfering RNAs), and piRNAs (Piwi-interacting RNAs) are some elements that characterized the group of noncoding small RNAs, and the main differences between them are their molecular origin, biogenesis course, and size (for review see [1, 2]). These tiny molecules participate directly in gene expression outcome by physical interaction with mRNAs [3] and indirectly through aiding heterochromatin formation [4]. Therefore, due to their ability in interfering in transcriptome, small RNAs virtually participate on all biological processes. piRNAs and siRNAs seem to be important in gametogenesis and retrotransposon silencing of mammalian germ line [5, 6], as well as embryo development. Recently,

References

[1]  V. N. Kim, J. Han, and M. C. Siomi, “Biogenesis of small RNAs in animals,” Nature Reviews Molecular Cell Biology, vol. 10, no. 2, pp. 126–139, 2009.
[2]  L. He and G. J. Hannon, “MicroRNAs: small RNAs with a big role in gene regulation,” Nature Reviews Genetics, vol. 5, no. 7, pp. 522–531, 2004.
[3]  D. P. Bartel, “MicroRNAs: genomics, biogenesis, mechanism, and function,” Cell, vol. 116, no. 2, pp. 281–297, 2004.
[4]  T. Volpe and R. A. Martienssen, “RNA interference and heterochromatin assembly,” Cold Spring Harbor Perspectives in Biology. In press.
[5]  T. Watanabe, Y. Totoki, A. Toyoda et al., “Endogenous siRNAs from naturally formed dsRNAs regulate transcripts in mouse oocytes,” Nature, vol. 453, no. 7194, pp. 539–543, 2008.
[6]  S. Kuramochi-Miyagawa, T. Watanabe, K. Gotoh et al., “DNA methylation of retrotransposon genes is regulated by Piwi family members MILI and MIWI2 in murine fetal testes,” Genes and Development, vol. 22, no. 7, pp. 908–917, 2008.
[7]  Y. Ohnishi, Y. Totoki, A. Toyoda et al., “Small RNA class transition from siRNA/piRNA to miRNA during pre-implantation mouse development,” Nucleic Acids Research, vol. 38, no. 15, pp. 5141–5151, 2010.
[8]  R. C. Lee, R. L. Feinbaum, and V. Ambros, “The C. elegans heterochronic gene lin-4 encodes small RNAs with antisense complementarity to lin-14,” Cell, vol. 75, no. 5, pp. 843–854, 1993.
[9]  Q. Liu and Z. Paroo, “Biochemical principles of small RNA pathways,” Annual Review of Biochemistry, vol. 79, pp. 295–319, 2010.
[10]  D. P. Bartel, “MicroRNAs: target recognition and regulatory functions,” Cell, vol. 136, no. 2, pp. 215–233, 2009.
[11]  B. P. Lewis, C. B. Burge, and D. P. Bartel, “Conserved seed pairing, often flanked by adenosines, indicates that thousands of human genes are microRNA targets,” Cell, vol. 120, no. 1, pp. 15–20, 2005.
[12]  S. Mocellin, S. Pasquali, and P. Pilati, “Oncomirs: from tumor biology to molecularly targeted anticancer strategies,” Mini-Reviews in Medicinal Chemistry, vol. 9, no. 1, pp. 70–80, 2009.
[13]  H. Tsao, V. Goel, H. Wu, G. Yang, and F. G. Haluska, “Genetic interaction between NRAS and BRAF mutations and PTEN/MMAC1 inactivation in melanoma,” Journal of Investigative Dermatology, vol. 122, no. 2, pp. 337–341, 2004.
[14]  K. D. Meyle and P. Guldberg, “Genetic risk factors for melanoma,” Human Genetics, vol. 126, no. 4, pp. 499–510, 2009.
[15]  J. Y. Lin and D. E. Fisher, “Melanocyte biology and skin pigmentation,” Nature, vol. 445, no. 7130, pp. 843–850, 2007.
[16]  N. F. Box and T. Terzian, “The role of p53 in pigmentation, tanning and melanoma,” Pigment Cell and Melanoma Research, vol. 21, no. 5, pp. 525–533, 2008.
[17]  M. Nihal, C. T. Roelke, and G. S. Wood, “Anti-melanoma effects of vorinostat in combination with polyphenolic antioxidant (-)-epigallocatechin-3-gallate (EGCG),” Pharmaceutical Research, vol. 27, no. 6, pp. 1103–1114, 2010.
[18]  R. C. Howell, E. Revskaya, V. Pazo, J. D. Nosanchuk, A. Casadevall, and E. Dadachova, “Phage display library derived peptides that bind to human tumor melanin as potential vehicles for targeted radionuclide therapy of metastatic melanoma,” Bioconjugate Chemistry, vol. 18, no. 6, pp. 1739–1748, 2007.
[19]  C. Garbe and T. K. Eigentler, “Diagnosis and treatment of cutaneous melanoma: state of the art 2006,” Melanoma Research, vol. 17, no. 2, pp. 117–127, 2007.
[20]  V. Gray-Schopfer, C. Wellbrock, and R. Marais, “Melanoma biology and new targeted therapy,” Nature, vol. 445, no. 7130, pp. 851–857, 2007.
[21]  P. M. Howell, S. Liu, S. Ren, C. Behlen, O. Fodstad, and A. I. Riker, “Epigenetics in human melanoma,” Cancer Control, vol. 16, no. 3, pp. 200–218, 2009.
[22]  V. Ambros, “The functions of animal microRNAs,” Nature, vol. 431, no. 7006, pp. 350–355, 2004.
[23]  T. Kawamata and Y. Tomari, “Making RISC,” Trends in Biochemical Sciences, vol. 35, no. 7, pp. 368–376, 2010.
[24]  G. M. Borchert, W. Lanier, and B. L. Davidson, “RNA polymerase III transcribes human microRNAs,” Nature Structural and Molecular Biology, vol. 13, no. 12, pp. 1097–1101, 2006.
[25]  G. A. Calin, C. Sevignani, C. D. Dumitru et al., “Human microRNA genes are frequently located at fragile sites and genomic regions involved in cancers,” Proceedings of the National Academy of Sciences of the United States of America, vol. 101, no. 9, pp. 2999–3004, 2004.
[26]  F. Molognoni, A. T. Cruz, F. M. Meliso et al., “Epigenetic reprogramming as a key contributor to melanocyte malignant transformation,” Epigenetics, vol. 6, no. 4, pp. 451–465, 2011.
[27]  S. A. Melo, C. Moutinho, S. Ropero et al., “A genetic defect in exportin-5 traps precursor MicroRNAs in the nucleus of cancer cells,” Cancer Cell, vol. 18, no. 4, pp. 303–315, 2010.
[28]  J. B. Cowland, C. Hother, and K. Gr?nb?K, “MicroRNAs and cancer,” Acta Pathologica, Microbiologica et Immunologica Scandinavica, vol. 115, no. 10, pp. 1090–1106, 2007.
[29]  Y. Wang, R. Medvid, C. Melton, R. Jaenisch, and R. Blelloch, “DGCR8 is essential for microRNA biogenesis and silencing of embryonic stem cell self-renewal,” Nature Genetics, vol. 39, no. 3, pp. 380–385, 2007.
[30]  B. Muralidhar, L. D. Goldstein, G. Ng et al., “Global microRNA profiles in cervical squamous cell carcinoma depend on Drosha expression levels,” Journal of Pathology, vol. 212, no. 4, pp. 368–377, 2007.
[31]  N. Sugito, H. Ishiguro, Y. Kuwabara et al., “RNASEN regulates cell proliferation and affects survival in esophageal cancer patients,” Clinical Cancer Research, vol. 12, no. 24, pp. 7322–7328, 2006.
[32]  G. Meister and T. Tuschl, “Mechanisms of gene silencing by double-stranded RNA,” Nature, vol. 431, no. 7006, pp. 343–349, 2004.
[33]  L. Zhang, J. Huang, N. Yang et al., “microRNAs exhibit high frequency genomic alterations in human cancer,” Proceedings of the National Academy of Sciences of the United States of America, vol. 103, no. 24, pp. 9136–9141, 2006.
[34]  R. I. Gregory and R. Shiekhattar, “MicroRNA biogenesis and cancer,” Cancer Research, vol. 65, no. 9, pp. 3509–3512, 2005.
[35]  M. P. Perron and P. Provost, “Protein components of the microRNA pathway and human diseases,” Methods in Molecular Biology, vol. 487, pp. 369–385, 2009.
[36]  E. Berezikov, W. J. Chung, J. Willis, E. Cuppen, and E. C. Lai, “Mammalian mirtron genes,” Molecular Cell, vol. 28, no. 2, pp. 328–336, 2007.
[37]  C. Levy, M. Khaled, K. C. Robinson et al., “Lineage-specific transcriptional regulation of DICER by MITF in melanocytes,” Cell, vol. 141, no. 6, pp. 994–1005, 2010.
[38]  M. Sand, T. Gambichler, D. Sand, P. Altmeyer, M. Stuecker, and F. G. Bechara, “Immunohistochemical expression patterns of the microRNA-processing enzyme Dicer in cutaneous malignant melanomas, benign melanocytic nevi and dysplastic melanocytic nevi,” European Journal of Dermatology, vol. 21, no. 1, pp. 18–21, 2011.
[39]  A. D. Haase, L. Jaskiewicz, H. Zhang et al., “TRBP, a regulator of cellular PKR and HIV-1 virus expression, interacts with Dicer and functions in RNA silencing,” EMBO Reports, vol. 6, no. 10, pp. 961–967, 2005.
[40]  Y. Lee, I. Hur, S. Y. Park, Y. K. Kim, R. S. Mi, and V. N. Kim, “The role of PACT in the RNA silencing pathway,” EMBO Journal, vol. 25, no. 3, pp. 522–532, 2006.
[41]  M. Trabucchi, P. Briata, M. Garcia-Mayoral et al., “The RNA-binding protein KSRP promotes the biogenesis of a subset of microRNAs,” Nature, vol. 459, no. 7249, pp. 1010–1014, 2009.
[42]  S. A. Melo, S. Ropero, C. Moutinho et al., “A TARBP2 mutation in human cancer impairs microRNA processing and DICER1 function,” Nature Genetics, vol. 41, no. 3, pp. 365–370, 2009.
[43]  M. Benkirane, C. Neuveut, R. F. Chun et al., “Oncogenic potential of TAR RNA binding protein TRBP and its regulatory interaction with RNA-dependent protein kinase PKR,” EMBO Journal, vol. 16, no. 3, pp. 611–624, 1997.
[44]  L. Boominathan, “The tumor suppressors p53, p63, and p73 are regulators of microRNA processing complex,” PLoS One, vol. 5, no. 5, Article ID e10615, 2010.
[45]  I. Rigoutsos, “New tricks for animal micrornas: targeting of amino acid coding regions at conserved and nonconserved sites,” Cancer Research, vol. 69, no. 8, pp. 3245–3248, 2009.
[46]  B. N. Davis-Dusenbery and A. Hata, “Mechanisms of control of microRNA biogenesis,” Journal of Biochemistry, vol. 148, no. 4, pp. 381–392, 2010.
[47]  B. D. Adams, K. P. Claffey, and B. A. White, “Argonaute-2 expression is regulated by epidermal growth factor receptor and mitogen-activated protein kinase signaling and correlates with a transformed phenotype in breast cancer cells,” Endocrinology, vol. 150, no. 1, pp. 14–23, 2009.
[48]  D. C. Bennett, “How to make a melanoma: what do we know of the primary clonal events?” Pigment Cell and Melanoma Research, vol. 21, no. 1, pp. 27–38, 2008.
[49]  A. J. Miller and M. C. Mihm Jr., “Melanoma,” New England Journal of Medicine, vol. 355, no. 1, pp. 51–65, 2006.
[50]  A. Tang, M. S. Eller, M. Hara, M. Yaar, S. Hirohashi, and B. A. Gilchrest, “E-cadherin is the major mediator of human melanocyte adhesion to keratinocytes in vitro,” Journal of Cell Science, vol. 107, no. 4, pp. 983–992, 1994.
[51]  K. Satyamoorthy and M. Herlyn, “Cellular and molecular biology of human melanoma,” Cancer Biology & Therapy, vol. 1, no. 1, pp. 14–17, 2002.
[52]  N. K. Haass and M. Herlyn, “Normal human melanocyte homeostasis as a paradigm for understanding melanoma,” The Journal of Investigative Dermatology Symposium Proceedings, vol. 10, no. 2, pp. 153–163, 2005.
[53]  D. W. Mueller and A. K. Bosserhoff, “MicroRNA miR-196a controls melanoma-associated genes by regulating HOX-C8 expression,” International Journal of Cancer, vol. 129, no. 5, pp. 1064–1074, 2011.
[54]  M. C. Magli, P. Barba, A. Celetti, G. De Vita, C. Cillo, and E. Boncinelli, “Coordinate regulation of HOX genes in human hematopoietic cells,” Proceedings of the National Academy of Sciences of the United States of America, vol. 88, no. 14, pp. 6348–6352, 1991.
[55]  S. Yekta, I. H. Shih, and D. P. Bartel, “MicroRNA-directed cleavage of HOXB8 mRNA,” Science, vol. 304, no. 5670, pp. 594–596, 2004.
[56]  J. P. Their, “Epithelial-mesenchymal transitions in tumor progression,” Nature Reviews Cancer, vol. 2, no. 6, pp. 442–454, 2002.
[57]  S. Brabletz and T. Brabletz, “The ZEB/miR-200 feedback loop-a motor of cellular plasticity in development and cancer?” EMBO Reports, vol. 11, no. 9, pp. 670–677, 2010.
[58]  U. Burk, J. Schubert, U. Wellner et al., “A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells,” EMBO Reports, vol. 9, no. 6, pp. 582–589, 2008.
[59]  P. A. Gregory, A. G. Bert, E. L. Paterson et al., “The miR-200 family and miR-205 regulate epithelial to mesenchymal transition by targeting ZEB1 and SIP1,” Nature Cell Biology, vol. 10, no. 5, pp. 593–601, 2008.
[60]  D. W. Mueller, M. Rehli, and A. K. Bosserhoff, “miRNA expression profiling in melanocytes and melanoma cell lines reveals miRNAs associated with formation and progression of malignant melanoma,” Journal of Investigative Dermatology, vol. 129, no. 7, pp. 1740–1751, 2009.
[61]  J. Schultz, P. Lorenz, G. Gross, S. Ibrahim, and M. Kunz, “MicroRNA let-7b targets important cell cycle molecules in malignant melanoma cells and interferes with anchorage-independent growth,” Cell Research, vol. 18, no. 5, pp. 549–557, 2008.
[62]  N. Rosenfeld, R. Aharonov, E. Meiri et al., “MicroRNAs accurately identify cancer tissue origin,” Nature Biotechnology, vol. 26, no. 4, pp. 462–469, 2008.
[63]  I. Elson-Schwab, A. Lorentzen, and C. J. Marshall, “MicroRNA-200 family members differentially regulate morphological plasticity and mode of melanoma cell invasion,” PLoS One, vol. 5, no. 10, 2010.
[64]  C. A. Hodgkinson, K. J. Moore, A. Nakayama et al., “Mutations at the mouse microphthalmia locus are associated with defects in a gene encoding a novel basic-helix-loop-helix-zipper protein,” Cell, vol. 74, no. 2, pp. 395–404, 1993.
[65]  K. I. Yasumoto, K. Yokoyama, K. Shibata, Y. Tomita, and S. Shibahara, “Microphthalmia-associated transcription factor as a regulator for melanocyte-specific transcription of the human tyrosinase gene,” Molecular and Cellular Biology, vol. 14, no. 12, pp. 8058–8070, 1994.
[66]  J. Vachtenheim and J. Borovansky, “"Transcription physiology" of pigment formation in melanocytes: central role of MITF,” Experimental Dermatology, vol. 19, no. 7, pp. 617–627, 2010.
[67]  L. A. Garraway, H. R. Widlund, M. A. Rubin et al., “Integrative genomic analyses identify MITF as a lineage survival oncogene amplified in malignant melanoma,” Nature, vol. 436, no. 7047, pp. 117–122, 2005.
[68]  M. F. Segura, D. Hanniford, S. Menendez et al., “Aberrant miR-182 expression promotes melanoma metastasis by repressing FOXO3 and microphthalmia-associated transcription factor,” Proceedings of the National Academy of Sciences of the United States of America, vol. 106, no. 6, pp. 1814–1819, 2009.
[69]  B. S. Haflidadóttir, K. Bergsteinsdóttir, C. Praetorius, and E. Steingrímsson, “miR-148 regulates Mitf in melanoma cells,” PLoS One, vol. 5, no. 7, Article ID e11574, 2010.
[70]  L. T. Bemis, R. Chen, C. M. Amato et al., “MicroRNA-137 targets microphthalmia-associated transcription factor in melanoma cell lines,” Cancer Research, vol. 68, no. 5, pp. 1362–1368, 2008.
[71]  M. Bloch, J. Ousingsawat, R. Simon et al., “KCNMA1 gene amplification promotes tumor cell proliferation in human prostate cancer,” Oncogene, vol. 26, no. 17, pp. 2525–2534, 2007.
[72]  A. J. Miller, J. Du, S. Rowan, C. L. Hershey, H. R. Widlund, and D. E. Fisher, “Transcriptional regulation of the melanoma prognostic marker melastatin (TRPM1) by MITF in melanocytes and melanoma,” Cancer Research, vol. 64, no. 2, pp. 509–516, 2004.
[73]  J. Mazar, K. de Young, D. Khaitan et al., “The regulation of miRNA-211 expression and its role in melanoma cell invasiveness,” PLoS One, vol. 5, no. 11, Article ID e13779, 2010.
[74]  J. Chen, H. E. Feilotter, G. C. Paré et al., “MicroRNA-193b represses cell proliferation and regulates cyclin D1 in melanoma,” American Journal of Pathology, vol. 176, no. 5, pp. 2520–2529, 2010.
[75]  D. Philippidou, M. Schmitt, D. Moser et al., “Signatures of MicroRNAs and selected MicroRNA target genes in human melanoma,” Cancer Research, vol. 70, no. 10, pp. 4163–4173, 2010.
[76]  S. M. Johnson, H. Grosshans, J. Shingara et al., “RAS is regulated by the let-7 microRNA family,” Cell, vol. 120, no. 5, pp. 635–647, 2005.
[77]  M. E. Peter, “Let-7 and miR-200 microRNAs: guardians against pluripotency and cancer progression,” Cell Cycle, vol. 8, no. 6, pp. 843–852, 2009.
[78]  E. R. Sauter, U. C. Yeo, A. Von Stemm et al., “Cyclin D1 is a candidate oncogene in cutaneous melanoma,” Cancer Research, vol. 62, no. 11, pp. 3200–3206, 2002.
[79]  A. A. Dar, S. Majid, D. De Semir, M. Nosrati, V. Bezrookove, and M. Kashani-Sabet, “miRNA-205 suppresses melanoma cell proliferation and induces senescence via regulation of E2F1 protein,” Journal of Biological Chemistry, vol. 286, no. 19, pp. 16606–16614, 2011.
[80]  R. Hoekstra, F. A. L. M. Eskens, and J. Verweij, “Matrix metalloproteinase inhibitors: current developments and future perspectives,” Oncologist, vol. 6, no. 5, pp. 415–427, 2001.
[81]  T.-Y. Fu, C.-C. Chang, C.-T. Lin et al., “Let-7b-mediated suppression of basigin expression and metastasis in mouse melanoma cells,” Experimental Cell Research, vol. 317, no. 4, pp. 445–451, 2011.
[82]  C. P. Walsh and T. H. Bestor, “Cytosine methylation and mammalian development,” Genes and Development, vol. 13, no. 1, pp. 26–34, 1999.
[83]  J. T. Attwood, R. L. Yung, and B. C. Richardson, “DNA methylation and the regulation of gene transcription,” Cellular and Molecular Life Sciences, vol. 59, no. 2, pp. 241–257, 2002.
[84]  P. Siedlecki and P. Zielenkiewicz, “Mammalian DNA methyltransferases,” Acta Biochimica Polonica, vol. 53, no. 2, pp. 245–256, 2006.
[85]  E. N. Gal-Yam, Y. Saito, G. Egger, and P. A. Jones, “Cancer epigenetics: modifications, screening, and therapy,” Annual Review of Medicine, vol. 59, pp. 267–280, 2008.
[86]  M. W. ?uczak and P. P. Jagodziński, “The role of DNA methylation in cancer development,” Folia Histochemica et Cytobiologica, vol. 44, no. 3, pp. 143–154, 2006.
[87]  R. Brown and G. Strathdee, “Epigenomics and epigenetic therapy of cancer,” Trends in Molecular Medicine, vol. 8, no. 4, pp. S43–S48, 2002.
[88]  M. Okano, D. W. Bell, D. A. Haber, and E. Li, “DNA methyltransferases Dnmt3a and Dnmt3b are essential for de novo methylation and mammalian development,” Cell, vol. 99, no. 3, pp. 247–257, 1999.
[89]  G. L. Xu, T. H. Bestor, D. Bourc'his et al., “Chromosome instability and immunodeficiency syndrome caused by mutations in a DNA methyltransferase gene,” Nature, vol. 402, no. 6758, pp. 187–191, 1999.
[90]  R. K. Lin, H. S. Hsu, J. W. Chang, C. Y. Chen, J. T. Chen, and YI. C. Wang, “Alteration of DNA methyltransferases contributes to 5′CpG methylation and poor prognosis in lung cancer,” Lung Cancer, vol. 55, no. 2, pp. 205–213, 2007.
[91]  C. Braconi, N. Huang, and T. Patel, “Microrna-dependent regulation of DNA methyltransferase-1 and tumor suppressor gene expression by interleukin-6 in human malignant cholangiocytes,” Hepatology, vol. 51, no. 3, pp. 881–890, 2010.
[92]  F. Meng, Y. Yamagiwa, Y. Ueno, and T. Patel, “Over-expression of interleukin-6 enhances cell survival and transformed cell growth in human malignant cholangiocytes,” Journal of Hepatology, vol. 44, no. 6, pp. 1055–1065, 2006.
[93]  A. M. Duursma, M. Kedde, M. Schrier, C. Le Sage, and R. Agami, “miR-148 targets human DNMT3b protein coding region,” RNA, vol. 14, no. 5, pp. 872–877, 2008.
[94]  M. Fabbri, R. Garzon, A. Cimmino et al., “MicroRNA-29 family reverts aberrant methylation in lung cancer by targeting DNA methyltransferases 3A and 3B,” Proceedings of the National Academy of Sciences of the United States of America, vol. 104, no. 40, pp. 15805–15810, 2007.
[95]  L. Han, P. D. Witmer, E. Casey, D. Valle, and S. Sukumar, “DNA methylation regulates microRNA expression,” Cancer Biology and Therapy, vol. 6, no. 8, pp. 1284–1288, 2007.
[96]  D. Lodygin, V. Tarasov, A. Epanchintsev et al., “Inactivation of miR-34a by aberrant CpG methylation in multiple types of cancer,” Cell Cycle, vol. 7, no. 16, pp. 2591–2600, 2008.
[97]  X. He, L. He, and G. J. Hannon, “The guardian's little helper: microRNAs in the p53 tumor suppressor network,” Cancer Research, vol. 67, no. 23, pp. 11099–11101, 2007.
[98]  B. Brueckner, C. Stresemann, R. Kuner et al., “The human let-7a-3 locus contains an epigenetically regulated microRNA gene with oncogenic function,” Cancer Research, vol. 67, no. 4, pp. 1419–1423, 2007.
[99]  S. J. Vidwans, K. T. Flaherty, D. E. Fisher, J. M. Tenenbaum, M. D. Travers, and J. Shrager, “A melanoma molecular disease model,” PLoS One, vol. 6, no. 3, Article ID e18257, 2011.
[100]  V. A. Krutovskikh and Z. Herceg, “Oncogenic microRNAs (OncomiRs) as a new class of cancer biomarkers,” BioEssays, vol. 32, no. 10, pp. 894–904, 2010.
[101]  P. S. Mitchell, R. K. Parkin, E. M. Kroh et al., “Circulating microRNAs as stable blood-based markers for cancer detection,” Proceedings of the National Academy of Sciences of the United States of America, vol. 105, no. 30, pp. 10513–10518, 2008.
[102]  M. Osaki, F. Takeshita, and T. Ochiya, “MicroRNAs as biomarkers and therapeutic drugs in human cancer,” Biomarkers, vol. 13, no. 7-8, pp. 658–670, 2008.
[103]  L. M. B. Holst, B. Kaczkowski, M. Glud, E. Futoma-Kazmierczak, L. F. Hansen, and R. Gniadecki, “The microRNA molecular signature of atypic and common acquired melanocytic nevi: differential expression of miR-125b and let-7c,” Experimental Dermatology, vol. 20, no. 3, pp. 278–280, 2011.
[104]  M. Scatolini, M. M. Grand, E. Grosso et al., “Altered molecular pathways in melanocytic lesions,” International Journal of Cancer, vol. 126, no. 8, pp. 1869–1881, 2010.
[105]  M. Glud, M. Rossing, C. Hother et al., “Downregulation of miR-125b in metastatic cutaneous malignant melanoma,” Melanoma Research, vol. 20, no. 6, pp. 479–484, 2010.
[106]  F. Felicetti, M. C. Errico, L. Bottero et al., “The promyelocytic leukemia zinc finger-microRNA-221/-222 pathway controls melanoma progression through multiple oncogenic mechanisms,” Cancer Research, vol. 68, no. 8, pp. 2745–2754, 2008.
[107]  H. Kanemaru, S. Fukushima, J. Yamashita et al., “The circulating microRNA-221 level in patients with malignant melanoma as a new tumor marker,” Journal of Dermatological Science, vol. 61, no. 3, pp. 187–193, 2011.
[108]  S. A. Ciafrè, S. Galardi, A. Mangiola et al., “Extensive modulation of a set of microRNAs in primary glioblastoma,” Biochemical and Biophysical Research Communications, vol. 334, no. 4, pp. 1351–1358, 2005.
[109]  C. Z. Zhang, L. Han, A. L. Zhang et al., “MicroRNA-221 and microRNA-222 regulate gastric carcinoma cell proliferation and radioresistance by targeting PTEN,” BMC Cancer, vol. 10, p. 367, 2010.
[110]  C. Huynh, M. F. Segura, A. Gaziel-Sovran et al., “Efficient in vivo microRNA targeting of liver metastasis,” Oncogene, vol. 30, no. 12, pp. 1481–1488, 2011.

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