Please use this identifier to cite or link to this item:
|Title:||Protein tyrosine phosphatase UBASH3B is overexpressed in triple-negative breast cancer and promotes invasion and metastasis|
|Citation:||Lee, S.T., Feng, M., Wei, Y., Li, Z., Qiao, Y., Guan, P., Jiang, X., Wong, C.H., Huynh, K., Wang, J., Li, J., Karuturi, K.M., Tan, E.Y., Hoon, D.S.B., Kang, Y., Yu, Q. (2013-07-02). Protein tyrosine phosphatase UBASH3B is overexpressed in triple-negative breast cancer and promotes invasion and metastasis. Proceedings of the National Academy of Sciences of the United States of America 110 (27) : 11121-11126. ScholarBank@NUS Repository. https://doi.org/10.1073/pnas.1300873110|
|Abstract:||Efforts to improve the clinical outcome of highly aggressive triple-negative breast cancer (TNBC) have been hindered by the lack of effective targeted therapies. Thus, it is important to identify the specific gene targets/pathways driving the invasive phenotype to develop more effective therapeutics. Here we show that ubiquitin-associated and SH3 domain-containing B (UBASH3B), a protein tyrosine phosphatase, is overexpressed in TNBC, where it supports malignant growth, invasion, and metastasis largely through modulating epidermal growth factor receptor (EGFR). We also show that UBASH3B is a functional target of anti-invasive microRNA200a (miR200a) that is down-regulated in TNBC. Importantly, the oncogenic potential of UBASH3B is dependent on its tyrosine phosphatase activity, which targets CBL ubiquitin ligase for dephosphorylation and inactivation, leading to EGFR up-regulation. Thus, UBASH3B may function as a crucial node in bridging multiple invasion-promoting pathways, thereby providing a potential therapeutic target for TNBC.|
|Source Title:||Proceedings of the National Academy of Sciences of the United States of America|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on May 19, 2018
WEB OF SCIENCETM
checked on Apr 3, 2018
checked on Apr 19, 2018
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.