Abstract
The role of transglutaminase II (TGase II) in hyaluronic acid (HA)-promoted melanoma cell motility was investigated. HA induced the expression of TGase II via the nuclear factor κB (NF-kB) in melanoma cells. HA increased the Rac1 activity and phosphorylation of focal adhesion kinase (FAK). Transfection by lipofectamine of dominant-negative Rac1, and FAK-related non-kinase (FRNK), an endogenous inhibitor of FAK, suppressed the induction of TGase II. This suggests that Rac1 and FAK mediate induction of TGase II by HA. HA-promoted melanoma cell motility was inhibited by cystamine, an inhibitor of TGase II, and overexpression of TGase II enhanced melanoma cell motility through reactive oxygen species. Taken together, HA promotes melanoma cell motility through activation of Rac1, FAK, and induction of TGase II.
| Original language | English |
|---|---|
| Pages (from-to) | 31-39 |
| Number of pages | 9 |
| Journal | Biotechnology Letters |
| Volume | 30 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jan 2008 |
Bibliographical note
Funding Information:Acknowledgments This work was supported by grant (0103026-1-2) from the Basic Research Program of the Korea Science & Engineering Foundation, a grant from Korea Research Foundation and Vascular System Research Center, a grant from Korea Research Foundation (0805011-1-1), a grant from the 21C Frontier Functional Human Genome Project (FG06-2-23) from the Ministry of Science & Technology in Korea, and a grant (A050260) from the Ministry of Health and Welfare of Korea.
Keywords
- Focal adhesion kinase
- Hyaluronic acid
- Motility
- Rac1
- Transglutaminase II