Metastatic spread of tumor cells to vital organs is the major cause of death in 
cancer. Accumulating data support an important role of infiltrating immune cells 
in promoting carcinoma progression into metastatic disease. Tumor-infiltrating 
immune cells produce and secrete cytokines, growth factors and proteases that 
re-activate latent developmental processes including epithelial-mesenchymal 
transition (EMT). EMT provides tumor cells with invasive, migratory and stem 
cell properties allowing them to disseminate and propagate at distant sites. 
Induction of EMT requires two criteria to be fulfilled: (i) cells are competent 
to undergo EMT (ii) an EMT-permissive microenvironment exists. The cytokine 
TGF-β, which is expressed by tumor-infiltrating immune cells, stands out as a 
master regulator of the pro-invasive tumor microenvironment. TGF-β cooperates 
with stem cell pathways, such as Wnt and Ras signaling, to induce EMT. In 
addition, TGF-β contributes to an EMT-permissive microenvironment by switching 
the phenotypes of tumor-infiltrating immune cells, which thereby mount 
pro-invasive and pro-metastatic immune responses. In this review, we discuss the 
role of TGF-β-induced EMT as a link between cancer and inflammation in the 
context of questions, which from our point of view are key to answer in order to 
understand the functionality of EMT in tumors.