Microenvironmental Regulation of Epithelial-Mesenchymal Transitions in Cancer

被引:244
作者
Gao, Dingcheng [1 ,2 ,4 ]
Vahdat, Linda T. [3 ]
Wong, Stephen [5 ]
Chang, Jenny C. [5 ]
Mittal, Vivek [1 ,2 ,4 ]
机构
[1] Cornell Univ, Weill Cornell Med Coll, Dept Cardiothorac Surg, New York, NY 10065 USA
[2] Cornell Univ, Weill Cornell Med Coll, Dept Cell & Dev Biol, New York, NY 10065 USA
[3] Cornell Univ, Weill Cornell Med Coll, Dept Med, New York, NY 10065 USA
[4] Cornell Univ, Weill Cornell Med Coll, Neuberger Berman Lung Canc Res Ctr, New York, NY 10065 USA
[5] Methodist Hosp Canc Ctr, Houston, TX USA
关键词
NEGATIVE FEEDBACK LOOP; BREAST-CANCER; MIR-200; FAMILY; PROGENITOR CELLS; TUMOR-GROWTH; E-CADHERIN; METASTASIS; CARCINOMA; INVASION; ZEB1;
D O I
10.1158/0008-5472.CAN-12-1223
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The evolution of the cancer cell into a metastatic entity is the major cause of death in patients with cancer. Activation of the epithelial-to-mesenchymal transition (EMT) endows invasive and metastatic properties upon cancer cells that favor successful colonization of distal target organs. The observation that in many cancers distant metastases resemble the epithelial phenotype of primary tumors has led to speculation that the disseminated tumor cells recruited to the target organs undergo mesenchymal-to-epithelial transition ( MET). However, the MET cascade has not been recapitulated in vivo, and the cellular and molecular regulators that promote MET remain unknown. In a recent report, using a model of spontaneous breast cancer, we have shown that bone marrow-derived myeloid progenitor cells in the premetastatic lung secrete the proteoglycan versican, which induces MET of metastatic tumor cells and accelerates metastases. This review summarizes recent progress in MET research, outlines a unique paracrine cross-talk between the microenvironment and the cancer cells, which promotes tumor outgrowth in the metastatic organ, and discusses opportunities for novel antimetastatic approaches for cancer therapy. Cancer Res; 72(19); 4883-9. (c) 2012 AACR.
引用
收藏
页码:4883 / 4889
页数:7
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