Microenvironmental Regulation of Epithelial–Mesenchymal Transitions in Cancer
作者： Dingcheng Gao , Linda T. Vahdat , Stephen Wong , Jenny C. Chang , Vivek Mittal
DOI: 10.1158/0008-5472.CAN-12-1223
关键词: Epithelial–mesenchymal transition 、 Versican 、 Cancer stem cell 、 Paracrine signalling 、 Biology 、 Tumor microenvironment 、 Cancer cell 、 Internal medicine 、 Breast cancer 、 Oncology 、 Cancer
摘要: The evolution of the cancer cell into a metastatic entity is major cause death in patients with cancer. Activation epithelial-to-mesenchymal transition (EMT) endows invasive and properties upon cells that favor successful colonization distal target organs. observation many cancers distant metastases resemble epithelial phenotype primary tumors has led to speculation disseminated tumor recruited organs undergo mesenchymal-to-epithelial (MET). However, MET cascade not been recapitulated vivo, cellular molecular regulators promote remain unknown. In recent report, using model spontaneous breast cancer, we have shown bone marrow-derived myeloid progenitor premetastatic lung secrete proteoglycan versican, which induces accelerates metastases. This review summarizes progress research, outlines unique paracrine cross-talk between microenvironment cells, promotes outgrowth organ, discusses opportunities for novel antimetastatic approaches therapy.
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