Format

Send to

Choose Destination
Eur Rev Med Pharmacol Sci. 2016 Jul;20(13):2819-24.

LncRNA UCA1 promotes epithelial-mesenchymal transition (EMT) of breast cancer cells via enhancing Wnt/beta-catenin signaling pathway.

Author information

1
College of Life Sciences, Sichuan University, Chengdu, Sichuan, China. chihuawu@outlook.com.

Abstract

OBJECTIVE:

LncRNA UCA1 can promote invasion of breast cancer cells. However, the underlying mechanism is not quite clear. In this study, we investigated the regulative effect of UCA1 on the invasion capability of breast cancer cells and its association with the Wnt/β-catenin pathway.

MATERIALS AND METHODS:

Human breast cancer cell line MDA-MB-231 cells were transfected for UCA1 knockdown using UCA1 si-RNA. Transwell assay was performed to assess cell invasion capability. Western blot analysis was conducted to investigate the expression of mesenchymal and epithelial markers and the proteins involved in Wnt/beta-catenin signaling pathway. Immunofluorescent staining was further performed to verify the expression of E-cadherin and N-cadherin.

RESULTS:

MDA-MB-231 cells have strong invasion capability. Knockdown of endogenous UCA1 significantly reduced the number of invading cells. MDA-MB-231 cells with UCA1 knockdown had significantly increased expression of E-cadherin but decreased expression of N-cadherin, Vimentin and Snail. UCA1 inhibition substantially increased the expression of p-GSK-3β and GSK-3β and suppressed the protein expression of β-catenin and transcription of the downstream genes, including cyclin D1 and MMP-7.

CONCLUSIONS:

UCA1 can modulate epithelial-mesenchymal transition (EMT) of MDA-MB-231 cells and knockdown of UCA1 impaired the mesenchymal properties. UCA1 upregulation increases invasiveness of breast cancer cells at least partly via activating the Wnt/β-catenin signaling pathway.

PMID:
27424981
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for European Review for Medical and Pharmacological Sciences
Loading ...
Support Center