These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Long noncoding RNA DLX6-AS1 promotes breast cancer progression via miR-505-3p/RUNX2 axis. Author: Zhao P, Guan H, Dai Z, Ma Y, Zhao Y, Liu D. Journal: Eur J Pharmacol; 2019 Dec 15; 865():172778. PubMed ID: 31705901. Abstract: The dysregulation of long non-coding RNA (lncRNA) DLX6-AS1 has been identified to be involved in the development of several cancers, but its functional role and the underlying mechanism of DLX6-AS1 in breast cancer (BC) remains unknown. In the current study, the expression of DLX6-AS1 in the BC tissue samples was evaluated and the correlation between DLX6-AS1 expression and clinicopathological parameters were also analyzed. We found that DLX6-AS1 expression was much higher in tumor tissues than that in adjacent normal tissues and was positively associated with poor prognosis in BC patients. DLX6-AS1 knockdown significantly suppressed BC cell proliferation, invasion, migration, and promoted apoptosis. Moreover, luciferase reporter assay validated that DLX6-AS1 acted as an endogenous sponge to miR-505-3p and negatively regulated its expression. Additionally, miR-505-3p inhibited runt-related transcription factor 2 (RUNX2) expression by directly bind to its 3'- untranslated region (3'-UTR) and overexpression of RUNX2 partially reversed the effect of miR-505-3p mimics on BC cell proliferation and invasion. Furthermore, in BC tissues, miR-505-3p expression level was inversely associated with DLX6-AS1 and RUNX2, respectively. In conclusion, these findings demonstrated that DLX6-AS1 functioned as an oncogenic role that promoted BC proliferation and invasion through miR-505-3p/RUNX2 axis, which might serve as a potential therapeutic target for BC treatment.[Abstract] [Full Text] [Related] [New Search]