MicroRNA-driven deregulation of cytokine expression helps development of drug resistance in metastatic melanoma

被引:31
作者
Fattore, Luigi [1 ]
Sacconi, Andrea [2 ]
Mancini, Rita [3 ]
Ciliberto, Gennaro [4 ]
机构
[1] Natl Canc Inst Naples Fdn G Pascale, Naples, Italy
[2] Regina Elena Inst Canc Res, Translat Oncogen & Epigenet Unit, Rome, Italy
[3] Univ Roma Sapienza, Dept Mol & Clin Med, Rome, Italy
[4] Regina Elena Inst Canc Res, Rome, Italy
关键词
Melanoma; miRNA; Cytokines; Targeted therapies; Immunotherapy; MALIGNANT-MELANOMA; TUMOR-SUPPRESSOR; DOWN-REGULATION; MESENCHYMAL TRANSITION; ACQUIRED-RESISTANCE; BRAF; SURVIVAL; THERAPY; CANCER; PROGRESSION;
D O I
10.1016/j.cytogfr.2017.05.003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
microRNAs are major components of the eukaryotic post-transcriptional machinery and are frequently deregulated during cancer development. Increasing evidence points to them also as key players in the establishment of drug resistance. In this review, we provide an updated overview of the role of miRNAs in melanoma development and drug resistance and postulate that they are able to drive these processes in concert with deregulation of inflammatory and angiogenic cytokine expression. Notably, we have identified by querying the Cancer Genome Atlas database, a defined set of miRNAs which mostly have an impact on the development of melanoma and have recognized the main downstream pathways controlled by them. Most importantly, these miRNAs, which are down-regulated in metastatic melanomas as compared to primary tumors, are also able to predict prognosis of BRAF-mutated melanoma patients. Finally, we discuss the possibility that a common miRNA signature characterizes not only acquired resistance to MAPKi but also innate resistance to anti-PD-1 immunotherapy, since these conditions are both associated with alterations of the same pro-angiogenetic and pro-inflammatory pathways. (C) 2017 Elsevier Ltd. All rights reserved.
引用
收藏
页码:39 / 48
页数:10
相关论文
共 76 条
[21]   Activation of an early feedback survival loop involving phospho-ErbB3 is a general response of melanoma cells to RAF/MEK inhibition and is abrogated by anti-ErbB3 antibodies [J].
Fattore, Luigi ;
Marra, Emanuele ;
Pisanu, Maria Elena ;
Noto, Alessia ;
de Vitis, Claudia ;
Belleudi, Francesca ;
Aurisicchio, Luigi ;
Mancini, Rita ;
Torrisi, Maria Rosaria ;
Ascierto, Paolo Antonio ;
Ciliberto, Gennaro .
JOURNAL OF TRANSLATIONAL MEDICINE, 2013, 11
[22]   Exosome-mediated transfer of miR-222 is sufficient to increase tumor malignancy in melanoma [J].
Felicetti, Federica ;
De Feo, Alessandra ;
Coscia, Carolina ;
Puglisi, Rossella ;
Pedini, Francesca ;
Pasquini, Luca ;
Bellenghi, Maria ;
Errico, Maria Cristina ;
Pagani, Elena ;
Care, Alessandra .
JOURNAL OF TRANSLATIONAL MEDICINE, 2016, 14
[23]   Inhibition of Mutated, Activated BRAF in Metastatic Melanoma [J].
Flaherty, Keith T. ;
Puzanov, Igor ;
Kim, Kevin B. ;
Ribas, Antoni ;
McArthur, Grant A. ;
Sosman, Jeffrey A. ;
O'Dwyer, Peter J. ;
Lee, Richard J. ;
Grippo, Joseph F. ;
Nolop, Keith ;
Chapman, Paul B. .
NEW ENGLAND JOURNAL OF MEDICINE, 2010, 363 (09) :809-819
[24]   The mir-200 family and mir-205 regulate epithelial to mesenchymal transition by targeting ZEB1 and SIP1 [J].
Gregory, Philip A. ;
Bert, Andrew G. ;
Paterson, Emily L. ;
Barry, Simon C. ;
Tsykin, Anna ;
Farshid, Gelareh ;
Vadas, Mathew A. ;
Khew-Goodall, Yeesim ;
Goodall, Gregory J. .
NATURE CELL BIOLOGY, 2008, 10 (05) :593-601
[25]   Comparison of dabrafenib and trametinib combination therapy with vemurafenib monotherapy on health-related quality of life in patients with unresectable or metastatic cutaneous BRAF Val600-mutation-positive melanoma (COMBI-v): results of a phase 3, open-label, randomised trial [J].
Grob, Jean Jacques ;
Amonkar, Mayur M. ;
Karaszewska, Boguslawa ;
Schachter, Jacob ;
Dummer, Reinhard ;
Mackiewicz, Andrzej ;
Stroyakovskiy, Daniil ;
Drucis, Kamil ;
Grange, Florent ;
Chiarion-Sileni, Vanna ;
Rutkowski, Piotr ;
Lichinitser, Mikhail ;
Levchenko, Evgeny ;
Wolter, Pascal ;
Hauschild, Axel ;
Long, Georgina V. ;
Nathan, Paul ;
Ribas, Antoni ;
Flaherty, Keith ;
Sun, Peng ;
Legos, Jeffrey J. ;
McDowell, Diane Opatt ;
Mookerjee, Bijoyesh ;
Schadendorf, Dirk ;
Robert, Caroline .
LANCET ONCOLOGY, 2015, 16 (13) :1389-1398
[26]   Regulation of microRNA biogenesis [J].
Ha, Minju ;
Kim, V. Narry .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2014, 15 (08) :509-524
[27]   MicroRNAs in cancer: biomarkers, functions and therapy [J].
Hayes, Josie ;
Peruzzi, Pier Paolo ;
Lawler, Sean .
TRENDS IN MOLECULAR MEDICINE, 2014, 20 (08) :460-469
[28]   Genetic variation in the non-coding genome: Involvement of micro-RNAs and long non-coding RNAs in disease [J].
Hrdlickova, Barbara ;
de Almeida, Rodrigo Coutinho ;
Borek, Zuzanna ;
Withoff, Sebo .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 2014, 1842 (10) :1910-1922
[29]   Identification of a Tumor-Suppressive Human-Specific MicroRNA within the FHIT Tumor-Suppressor Gene [J].
Hu, Baocheng ;
Ying, Xiaomin ;
Wang, Jian ;
Piriyapongsa, Jittima ;
Jordan, I. King ;
Sheng, Jipo ;
Yu, Fang ;
Zhao, Po ;
Li, Yazhuo ;
Wang, Hongyan ;
Ng, Wooi Loon ;
Hu, Shuofeng ;
Wang, Xiang ;
Wang, Chenguang ;
Zheng, Xiaofei ;
Li, Wuju ;
Curran, Walter J. ;
Wang, Ya .
CANCER RESEARCH, 2014, 74 (08) :2283-2294
[30]   Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources [J].
Huang, Da Wei ;
Sherman, Brad T. ;
Lempicki, Richard A. .
NATURE PROTOCOLS, 2009, 4 (01) :44-57