Journal
TRANSLATIONAL RESEARCH
Volume 172, Issue -, Pages 45-60Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.trsl.2016.02.007
Keywords
-
Categories
Funding
- Swedish Cancer Foundation [130635]
- Swedish Research Council [B0434701]
- Soderberg Foundation [MN244/09]
- Skane University Hospital Research Foundation
- BioCare program at Lund University
- Gunnar Nilsson Cancer Foundation, Sweden
Ask authors/readers for more resources
Overexpression of wingless-type MMTV integration site family 5A (WNT5A) plays a significant role in melanoma cancer progression; however, the mechanism(s) involved remains unknown. In breast cancer, the human antigen R (HuR) has been implicated in the regulation of WNT5A expression. Here, we demonstrate that endogenous expression of WNT5A correlates with levels of active HuR in HTB63 and WM852 melanoma cells and that HuR binds to WNT5A messenger RNA in both cell lines. Although the HuR inhibitor MS-444 significantly impaired migration in both melanoma cell lines, it reduced WNT5A expression only in HTB63 cells, as did small interfering RNA knockdown of HuR. Consistent with this finding, MS-444-induced inhibition of HTB63 cell migration was restored by the addition of recombinant WNT5A, whereas MS-444-induced inhibition of WM852 cell migration was restored by the addition of recombinant matrix metalloproteinase-9, another HuR-regulated protein. Clearly, HuR positively regulates melanoma cell migration via at least 2 distinct mechanisms making HuR an attractive therapeutic target for halting melanoma dissemination.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available