Abstract
It has previously been reported that shedding of the PTPκ ectodomain drives enhanced motility of colon cancer cells. Herein, we provide mechanism underlying the regulation of PTPκ shedding by galectin-3 binding protein. PTPκ was inarguably scissored by the processed form of proprotein convertase 5 (subtilisin/kexin type 5), and galectin-3 binding protein which is over-produced in colon cancer cells and tissues contributed to increased cancer cell motility by acting as a negative regulator of galectin-3 at the cell surface. The high expression ratio of galectin-3 binding protein to galectin-3 was clinically correlated to lymphatic invasion. These results suggest that galectin-3 binding protein may be a potential therapeutic target for treatment of, at least, colon cancer patients with high expression of galectin-3 binding protein.
Original language | English |
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Pages (from-to) | 96-102 |
Number of pages | 7 |
Journal | Biochemical and Biophysical Research Communications |
Volume | 404 |
Issue number | 1 |
DOIs | |
State | Published - 7 Jan 2011 |
Bibliographical note
Funding Information:This work was supported by the ‘ Leading Foreign Research Institute Recruitment Program ’, the ‘Complex Carbohydrate Research Program’ and ‘ Convergence Research Center Program ( 2010K001115 )’ of the Ministry of Education, Science and Technology. Especially, we express deep appreciation to Daejeon metropolitan city for its support.
Keywords
- Galectin-3
- Galectin-3 binding protein
- Proprotein convertase 5
- PTPκ shedding