Loading…
Involvement of Cellular Prion Protein in Invasion and Metastasis of Lung Cancer by Inducing Treg Cell Development
The cellular prion protein (PrP ) is a cell surface glycoprotein expressed in many cell types that plays an important role in normal cellular processes. However, an increase in PrP expression has been associated with a variety of human cancers, where it may be involved in resistance to the prolifera...
Saved in:
Published in: | Biomolecules (Basel, Switzerland) Switzerland), 2021-02, Vol.11 (2), p.285 |
---|---|
Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | The cellular prion protein (PrP
) is a cell surface glycoprotein expressed in many cell types that plays an important role in normal cellular processes. However, an increase in PrP
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 (
) and PrP-overexpressing (Tga20) mice were studied to evaluate the role of PrP
in the invasion and metastasis of cancer. Tga20 mice, with increased PrP
, died more quickly from lung cancer than did the
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
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
plays an important role in invasion and metastasis of cancer cells by inducing Treg cells through upregulation of TGF-β and PD-L1 expression. |
---|---|
ISSN: | 2218-273X 2218-273X |
DOI: | 10.3390/biom11020285 |