Published September 2018 | Version v1
Journal article

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.2018.08.134

Additional 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.