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. Author manuscript; available in PMC: 2013 Jul 24.
Published in final edited form as: J Mammary Gland Biol Neoplasia. 2010 May 15;15(2):169–190. doi: 10.1007/s10911-010-9181-1

Figure 4.

Figure 4

Type 3 EMT in cancer metastasis. Normal epithelia that arose from type I EMT during development experience a carcinogenic event that ultimately results in their oncogenic transformation and tumor formation. The development and progression of mammary tumors is accompanied by their acquisition of dysplastic and abnormal morphologies, and by their evolution in chronically inflamed tumor microenvironments, which further enhances their acquisition of EMT and fibrotic phenotypes. Through its ability to stimulate oncogenic EMT, TGF-β enables transitioned mammary carcinoma cells to invade the underlying basement membrane (BM) and escape the confines of the primary tumor. Once liberated, metastatic MECs undergo intravasation and traverse the blood stream prior to taking up residence at distant locales, an event that ultimately leads to disease recurrence and poor clinical outcomes in breast cancer patients. See text for specific details on the molecular mechanisms whereby TGF-β promotes type 3 EMT and metastasis in breast cancer cells.