Cardiff University | Prifysgol Caerdydd ORCA
Online Research @ Cardiff 
WelshClear Cookie - decide language by browser settings

HuR, a key post-transcriptional regulator, and its implication in progression of breast cancer

Yuan, Zhu, Sanders, Andrew James ORCID:, Ye, Lin ORCID: and Jiang, Wen Guo ORCID: 2010. HuR, a key post-transcriptional regulator, and its implication in progression of breast cancer. Histology and Histopathology 25 (10) , pp. 1331-1340.

Full text not available from this repository.


HuR, an ubiquitously expressed member of the Hu family, selectively binds and stabilizes ARE-containing mRNAs encoding proto-oncogenes, cell cycle regulators, cytokines and growth factors. The mechanism of HuR stabilization on target mRNAs is believed to be mediated through competition with destabilizing ARE-BPs. HuR is mainly localized within the cell nucleus and the nucleo-cytoplasmic shuttling of HuR is generally assumed as the initial and critical step of its stabilizing effects. A number of signaling pathways are believed to be involved in HuR shuttling. Due to the pivotal role played by HuR in stabilizing the mRNA of key factors or cytokines involved in carcinogenesis and subsequent progression, its implication and therapeutic potential in cancer have been investigated intensively since its discovery in 1996. This review discusses the role of HuR in the stabilization of key mRNAs and it’s the nucleo-cytoplasmic shuttling. The review also covers the current knowledge of HuR’s role in carcinogenesis, particularly its involvement in breast cancer, and the feasibility of using HuR as a therapeutic target for the treatment of breast cancer.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Subjects: R Medicine > RC Internal medicine > RC0254 Neoplasms. Tumors. Oncology (including Cancer)
Uncontrolled Keywords: HuR; AU- and U-rich elements (AREs); nucleo-cytoplasmic shuttling; carcinogenesis; breast cancer
ISSN: 0213-3911
Last Modified: 19 Oct 2022 08:46

Citation Data

Cited 27 times in Scopus. View in Scopus. Powered By Scopus® Data

Actions (repository staff only)

Edit Item Edit Item