The miRNAs and Epithelial-Mesenchymal Transition in Cancers

被引:15
作者
Lin, Ching-Wen [1 ,2 ,3 ]
Kao, Shih-Han [1 ,2 ,3 ]
Yang, Pan-Chyr [1 ,2 ,3 ]
机构
[1] Acad Sinica, Inst Biomed Sci, Taipei 11529, Taiwan
[2] Natl Taiwan Univ, Natl Taiwan Univ Hosp, Dept Internal Med, Taipei 10764, Taiwan
[3] Natl Taiwan Univ, Coll Med, Taipei 10764, Taiwan
关键词
miRNAs; EMT; Epithelial-Mesenchymal Transition; cancers; E-CADHERIN EXPRESSION; SMAD-INTERACTING PROTEIN-1; REPRESSES E-CADHERIN; REGULATES E-CADHERIN; LOOP-HELIX PROTEINS; NF-KAPPA-B; TGF-BETA; TRANSCRIPTION FACTOR; UP-REGULATION; DOWN-REGULATION;
D O I
10.2174/1381612820666140128204508
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The epithelial-mesenchymal transition (EMT) is a process by which epithelial tumor cells acquire migratory and invasive abilities that enable them to spread to other organs. During this process, the tight junction molecule, E-cadherin, is often downregulated through transcription repression by the EMT-inducing transcription factors (EMT-TFs). MicroRNAs (miRNAs) are a class of small non-coding RNA molecules which bind to the complementary sequences within mRNA molecules. They post-transcriptionally govern gene silencing, thus affecting a broad range of physiological conditions, including EMT. In this review, we will discuss some well-known as well as brand-new EMT-related miRNAs and the signaling pathways in the tumor milieu that regulate their expressions and control cancer invasion and metastasis. Finally, we will discuss the application of miRNAs as therapeutic targets for treatment of cancer.
引用
收藏
页码:5309 / 5318
页数:10
相关论文
共 155 条
[1]   The tumour microenvironment as a target for chemoprevention [J].
Albini, Adriana ;
Sporn, Michael B. .
NATURE REVIEWS CANCER, 2007, 7 (02) :139-147
[2]   Role of the epithelial-mesenchymal transition regulator Slug in primary human cancers [J].
Alves, Catarina Castro ;
Carneiro, Fatima ;
Hoefler, Heinz ;
Becker, Karl-Friedrich .
FRONTIERS IN BIOSCIENCE-LANDMARK, 2009, 14 :3041-3050
[3]   Genome-Wide Epigenetic Regulation of miRNAs in Cancer [J].
Baer, Constance ;
Claus, Rainer ;
Plass, Christoph .
CANCER RESEARCH, 2013, 73 (02) :473-477
[4]   Crossroads of Wnt and Hippo in epithelial tissues [J].
Bernascone, Ilenia ;
Martin-Belmonte, Fernando .
TRENDS IN CELL BIOLOGY, 2013, 23 (08) :380-389
[5]   CADHERIN EXPRESSION IN CARCINOMAS - ROLE IN THE FORMATION OF CELL-JUNCTIONS AND THE PREVENTION OF INVASIVENESS [J].
BIRCHMEIER, W ;
BEHRENS, J .
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER, 1994, 1198 (01) :11-26
[6]   The transcription factor Slug represses E-cadherin expression and induces epithelial to mesenchymal transitions:: a comparison with Snail and E47 repressors [J].
Bolós, V ;
Peinado, H ;
Pérez-Moreno, MA ;
Fraga, MF ;
Esteller, M ;
Cano, A .
JOURNAL OF CELL SCIENCE, 2003, 116 (03) :499-511
[7]   EMT and induction of miR-21 mediate metastasis development in Trp53-deficient tumours [J].
Bornachea, Olga ;
Santos, Mirentxu ;
Belen Martinez-Cruz, Ana ;
Garcia-Escudero, Ramon ;
Duenas, Marta ;
Costa, Clotilde ;
Segrelles, Carmen ;
Lorz, Corina ;
Buitrago, Agueda ;
Saiz-Ladera, Cristina ;
Agirre, Xabier ;
Grande, Teresa ;
Paradela, Beatriz ;
Maraver, Antonio ;
Ariza, Jose M. ;
Prosper, Felipe ;
Serrano, Manuel ;
Sanchez-Cespedes, Montse ;
Paramio, Jesus M. .
SCIENTIFIC REPORTS, 2012, 2
[8]   The ZEB1/miR-200 feedback loop controls Notch signalling in cancer cells [J].
Brabletz, Simone ;
Bajdak, Karolina ;
Meidhof, Simone ;
Burk, Ulrike ;
Niedermann, Gabriele ;
Firat, Elke ;
Wellner, Ulrich ;
Dimmler, Arno ;
Faller, Gerhard ;
Schubert, Joerg ;
Brabletz, Thomas .
EMBO JOURNAL, 2011, 30 (04) :770-782
[9]   Downregulation of microRNAs directs the EMT and invasive potential of anaplastic thyroid carcinomas [J].
Braun, J. ;
Hoang-Vu, C. ;
Dralle, H. ;
Huettelmaier, S. .
ONCOGENE, 2010, 29 (29) :4237-4244
[10]   Aberrant expression of microRNAs involved in epithelial-mesenchymal transition of HT-29 cell line [J].
Cai, Zhi-Gang ;
Zhang, Shao-Ming ;
Zhang, Hang ;
Zhou, Yi-Yong ;
Wu, Hai-Bo ;
Xu, Xiao-Ping .
CELL BIOLOGY INTERNATIONAL, 2013, 37 (07) :669-674