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The cellular prion protein (PrP C ) is a cell surface glycoprotein expressed in many cell types that plays an important role in normal cellular processes. However, an increase in PrP C expression has been associated with a variety of human cancers, where it may be involved in resistance to the proliferation and metastasis of cancer cells. PrP-deficient ( Prnp 0/0  ) and PrP-overexpressing (Tga20) mice were studied to evaluate the role of PrP C in the invasion and metastasis of cancer. Tga20 mice, with increased PrP C , died more quickly from lung cancer than did the Prnp 0/0  mice, and this effect was associated with increased transforming growth factor-beta (TGF-β) and programmed death ligand-1 (PD-L1), which are important for the development and function of regulatory T (Treg) cells. The number of FoxP3 + CD25 + Treg cells was increased in Tga20 mice compared to Prnp 0/0  mice, but there was no significant difference in either natural killer or cytotoxic T cell numbers. In addition, mice infected with the ME7 scrapie strain had decreased numbers of Treg cells and decreased expression of TGF-β and PD-L1. These results suggest that PrP C plays an important role in invasion and metastasis of cancer cells by inducing Treg cells through upregulation of TGF-β and PD-L1 expression.

Involvement of Cellular Prion Protein in Invasion and Metastasis of Lung Cancer by Inducing Treg Cell Development