Androgen receptor suppresses prostate cancer cell invasion via altering the miR-4496/β-catenin signals
- 1. Department of Urology, Haikou People's Hospital, Xiangya Medical College Affiliated Haikou Hospital, Central South University, Haikou, Hainan, 570208 (China)
Description
Previous study found that AR in prostate may act as both a proliferator and a suppressor to promote or suppress the metastasis of prostate cancer (PCa). In current work, we demonstrated that AR could suppress PCa cell invasion through altering the miR-4496/β-catenin signals. And mechanisms dissection found that AR could negatively regulate the expression of β-catenin through enhancing the miR-4496 expression via directly binding to the AR-response-elements (AREs) of miR-4496 promoter, subsequently, the miRNA could directly target the 3' UTR of the β-catenin-mRNA to reduce its expression. To conclude, our work suggests that AR might play an important role to suppress PCa cell invasion, targeting the newly identified AR/miR-4496/β-catenin signaling with small molecules may help us to build up new therapeutic approaches to better suppress the metastasis of PCa.
Availability note (English)
Available from http://dx.doi.org/10.1016/j.bbrc.2018.08.134Additional details
Identifiers
- DOI
- 10.1016/j.bbrc.2018.08.134;
- PII
- S0006291X18318242;
Publishing Information
- Journal Title
- Biochemical and Biophysical Research Communications
- Journal Volume
- 504
- Journal Issue
- 1
- Journal Page Range
- p. 82-88
- ISSN
- 0006-291X
- CODEN
- BBRCA9
INIS
- Country of Publication
- United States
- Country of Input or Organization
- International Atomic Energy Agency (IAEA)
- INIS RN
- 53051446
- Subject category
- S60: APPLIED LIFE SCIENCES;
- Descriptors DEI
- ANDROGENS; MESSENGER-RNA; METASTASES; NEOPLASMS; PROSTATE; RECEPTORS
- Descriptors DEC
- ANDROSTANES; BODY; DISEASES; GLANDS; HORMONES; MALE GENITALS; MEMBRANE PROTEINS; NUCLEIC ACIDS; ORGANIC COMPOUNDS; ORGANS; PROTEINS; RNA; STEROID HORMONES; STEROIDS
Optional Information
- Copyright
- Copyright (c) 2018 Elsevier Inc. All rights reserved.