Upregulation of metastasis-associated PRL-3 initiates chordoma in zebrafish
- Li, L., Shi, H., Zhang, M., Guo, X., Tong, F., Zhang, W., Zhou, J., Wang, H., Yang, S.
- International Journal of Oncology 48(4): 1541-52 (Journal)
- Registered Authors
- Li, Li, Yang, Shulan
- MeSH Terms
- Cloning, Molecular
- Gene Expression Regulation, Developmental
- Gene Expression Regulation, Neoplastic
- Neoplasm Proteins/genetics*
- Neoplasm Proteins/metabolism*
- Protein Tyrosine Phosphatases/genetics*
- Protein Tyrosine Phosphatases/metabolism*
- Tissue Distribution
- Zebrafish/growth & development
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/metabolism*
- 26846972 Full text @ Int. J. Oncol.
Li, L., Shi, H., Zhang, M., Guo, X., Tong, F., Zhang, W., Zhou, J., Wang, H., Yang, S. (2016) Upregulation of metastasis-associated PRL-3 initiates chordoma in zebrafish. International Journal of Oncology. 48(4):1541-52.
The metastasis-associated phosphatase of regenerating liver-3 (PRL-3) plays multiple roles in progression of various human cancers; however, significance of its role during development has not been addressed. Here we cloned and characterized the expression pattern of zebrafish prl-3 transcript and showed that it is ubiquitiously expressed in the first 24 h of development with both maternal and zygotic expressions. The transcripts become progressively restricted to the notochord, vessels and the intestine by 96 h post-fertilization. Notably, overexpression of zebrafish Prl-3 (zPrl-3) and human PRL-3 induces notochord malformation in zebrafish. This phenotype resembles chordoma and is confirmed by associated misexpression of notochord-specific markers. Clinical significance of the PRL-3 in chordoma is strongly suggested by detection of PRL-3 antigen in clinical chordoma specimens. Collectively, our results uncovered that aberrant overexpression of PRL-3 could initiate chordoma in early development and suggest the use of PRL-3 could be used as a predictor and a therapeutic target for chordoma.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes