Epithelial-mesenchymal plasticity in carcinoma metastasis

被引:943
作者
Tsai, Jeff H. [1 ]
Yang, Jing [1 ,2 ]
机构
[1] Univ Calif San Diego, Sch Med, Dept Pharmacol, La Jolla, CA 92093 USA
[2] Univ Calif San Diego, Sch Med, Dept Pediat, La Jolla, CA 92093 USA
基金
美国国家卫生研究院;
关键词
epithelial-mesenchymal transition (EMT); mesenchymal-epithelial transition (MET); carcinoma metastasis; extravasation; intravasation; invasion; tumor dormancy; CIRCULATING TUMOR-CELLS; E-CADHERIN GENE; TRANSCRIPTION FACTOR SNAIL; NEGATIVE FEEDBACK LOOP; BREAST-CANCER CELLS; NF-KAPPA-B; MIR-200; FAMILY; COLORECTAL-CANCER; STEM-CELLS; INVADOPODIA FORMATION;
D O I
10.1101/gad.225334.113
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Tumor metastasis is a multistep process by which tumor cells disseminate from their primary site and form secondary tumors at a distant site. Metastasis occurs through a series of steps: local invasion, intravasation, transport, extravasation, and colonization. A developmental program termed epithelial-mesenchymal transition (EMT) has been shown to play a critical role in promoting metastasis in epithelium-derived carcinoma. Recent experimental and clinical studies have improved our knowledge of this dynamic program and implicated EMT and its reverse program, mesenchymal-epithelial transition (MET), in the metastatic process. Here, we review the functional requirement of EMT and/or MET during the individual steps of tumor metastasis and discuss the potential of targeting this program when treating metastatic diseases.
引用
收藏
页码:2192 / 2206
页数:15
相关论文
共 157 条
  • [1] Stem cell and epithelial-mesenchymal transition markers are frequently overexpressed in circulating tumor cells of metastatic breast cancer patients
    Aktas, Bahriye
    Tewes, Mitra
    Fehm, Tanja
    Hauch, Siegfried
    Kimmig, Rainer
    Kasimir-Bauer, Sabine
    [J]. BREAST CANCER RESEARCH, 2009, 11 (04)
  • [2] Prospective identification of tumorigenic breast cancer cells
    Al-Hajj, M
    Wicha, MS
    Benito-Hernandez, A
    Morrison, SJ
    Clarke, MF
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (07) : 3983 - 3988
  • [3] Induction of EMT by twist proteins as a collateral effect of tumor-promoting inactivation of premature senescence
    Ansieau, Stephane
    Bastid, Jeremy
    Doreau, Agnes
    Morel, Anne-Pierre
    Bouchet, Benjamin P.
    Thomas, Clemence
    Fauvet, Frederique
    Puisieux, Isabelle
    Doglioni, Claudio
    Piccinin, Sara
    Maestro, Roberta
    Voeltzel, Thibault
    Selmi, Abdelkader
    Valsesia-Wittmann, Sandrine
    de Fromentel, Claude Caron
    Puisieux, Alain
    [J]. CANCER CELL, 2008, 14 (01) : 79 - 89
  • [4] Glycogen synthase kinase-3 is an endogenous inhibitor of snail transcription: implications for the epithelial-mesenchymal transition
    Bachelder, RE
    Yoon, SO
    Franci, C
    de Herreros, AG
    Mercurio, AM
    [J]. JOURNAL OF CELL BIOLOGY, 2005, 168 (01) : 29 - 33
  • [5] Transcriptional activation of integrin β6 during the epithelial-mesenchymal transition defines a novel prognostic indicator of aggressive colon carcinoma
    Bates, RC
    Bellovin, DI
    Brown, C
    Maynard, E
    Wu, BY
    Kawakatsu, H
    Sheppard, D
    Oettgen, P
    Mercurio, AM
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 2005, 115 (02) : 339 - 347
  • [6] The transcription factor Snail is a repressor of E-cadherin gene expression in epithelial tumour cells
    Batlle, E
    Sancho, E
    Franci, C
    Domínguez, D
    Monfar, M
    Baulida, J
    de Herreros, AG
    [J]. NATURE CELL BIOLOGY, 2000, 2 (02) : 84 - 89
  • [7] BECKER KF, 1994, CANCER RES, V54, P3845
  • [8] Berx G, 1998, HUM MUTAT, V12, P226, DOI 10.1002/(SICI)1098-1004(1998)12:4<226::AID-HUMU2>3.0.CO
  • [9] 2-D
  • [10] E-cadherin is a tumour invasion suppressor gene mutated in human lobular breast cancers
    Berx, G
    CletonJansen, AM
    Nollet, F
    deLeeuw, WJF
    vandeVijver, MJ
    Cornelisse, C
    vanRoy, F
    [J]. EMBO JOURNAL, 1995, 14 (24) : 6107 - 6115