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 5;36(40):5620–5630. doi: 10.1038/onc.2017.170

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

Copyright © 2017 The Author(s)

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/

PMC Copyright notice

EphA2-deficiency impairs growth and progression in the C3-TAg transgenic model of basal-like breast cancer in vivo. We crossed C3-TAg mice with EphA2-deficient mice, generating a cohort of C3-TAg wild-type (EphA2^+/+), heterozygous (EphA2^+/−) and EphA2-deficient (EphA2-/-) mice. (a) EphA2-deficient mice formed significantly smaller tumors than wild-type or heterozygous littermates. (b) Tumor volume was significantly decreased in EphA2-deficient animals relative to littermate controls (N=9^+/+, 11^+/− and 9^−/− animals; *P<0.05, one-way ANOVA). (c) Morphometric analysis of hematoxylin and eosin-stained tumor sections revealed a significant decrease in mitotic figures (green arrowheads, a) in EphA2^−/− tumors relative to +/+ controls, as well as decreased cellularity (n=6 independent tumors/genotype; *P<0.05 Student’s t-test). (d) Histologic analyses of tumor sections for proliferation marker Ki67 revealed a significant decrease in proliferation index (%Ki67+ nuclei/total nuclei; *P<0.05, Student’s t-test) for EphA2^−/− tumors relative to controls. (e, f) Primary tumor cells from EphA2^+/+ and EphA2^−/− C3-TAg tumors were isolated and grown in three-dimensional spheroid cultures on Matrigel for 10–12 days. EphA2^−/− cells formed significantly smaller colonies than EphA2^+/+ cells (e, f; *P<0.05, Student’s t-test). Expression of EphA2 in EphA2^−/− cells via adenoviral transduction rescued colony size (e, f; *P<0.05, Student’s t-test) relative to adenovirus GFP control (expression confirmed by fluorescence analysis, lower right panel, e), restoring growth to near wild-type C3-TAg levels. N=3 independent experiments with triplicate biological replicates for each cell line. (g) EphA2-deficiency and overexpression of EphA2 following adenoviral transduction were confirmed by immunoblot analysis.