Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2017 Jun 28;7:4361. doi: 10.1038/s41598-017-04709-2

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

DACH1 regulated the expression of some CSCs and EMT genes in Met-1 cells and suppressed tumor growth in vivo. (a) Stable expression of DACH1 in breast cancer Met-1 cells was achieved by retrovirus infection. (b) RNA microarray and cluster analysis showed that upregulation of DACH1 reduced the mRNA levels of CD24, CD44, KLF4, MYC, FN1 and VIM in Met-1 cells. (c) Western blot indicated that upregulation of DACH1 reduced the protein abundance of CD44, Fibronectin, Vimentin, p21 and p27 in Met-1 cells. (d) DACH1 overexpression significantly reduced the volume of tumors by ∼90% and slowed down the speed of tumor growth in nude mice xenograft tumors. (e) Overexpression of DACH1 also reduced mice transplanted tumor weight by ∼90%. (f) Mammary tumor growth in vivo was evaluated by subcutaneous implantation of DACH1-overexpressing Met-1 cells and the GFP controls in nude mice.