Abstract
NCOA5 encodes a co-regulator for estrogen receptors (ERα and ERβ), orphan nuclear receptors (REV-ERBα and REV-ERBβ) and liver X receptor. It can influence many cellular processes by either promoting or inhibiting gene expression through its two important functional motifs: LxxLL (co-activator) and ΦxxΦΦ (co-repressor). Many reports have revealed the important roles of NCOA5 in diseases, such as diabetes, reproductive defects and autoimmune disease. In this review, we focus on its function in cancers and summary the current research progresses regarding its different roles in various cancers.
Highlights
Nuclear receptors (NRs) are a kind of transcriptional regulators that widely exist in animals
The cancer stem cell features of LM3 cells are diminished. These results revealed that even in the same tumor, Nuclear receptor co-activator 5 (NCOA5) might play different roles due to the difference of the tumor microenvironment
The mechanism of NCOA5 function in suppressing Hepatocellular carcinoma (HCC) has been dissected, we know little about its function and mechanism in other cancers
Summary
Nuclear receptors (NRs) are a kind of transcriptional regulators that widely exist in animals. At the C-terminal of LBD domain of NRs, there is a helical motif called activation function 2 (AF-2) which is responsible for co-regulator-receptor interaction. Like its dual functional capability in gene regulation, NCOA5 can play a role as a tumor promoter, and as a tumor suppressor, depending on the type of tissue.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.