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

. 2023 Jul 11;13:1161410. doi: 10.3389/fonc.2023.1161410

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

Copyright © 2023 Chen, Zhang, Liu, Chen, Zheng, Zhu and Zhang

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

A schematic representation of MMTV causing SBC in TA2 mice. TA2 mice transmit MMTV through breast milk or genetic material. TA2 mice with MMTV integrated into their DNA become pregnant several times and have active mammary epithelial cell division in response to estrogen and progesterone. Frequent DNA replication processes lead to the amplification of MMTV as well, and newly produced viral particles can infect mammary epithelial cells. Enhancer elements in viral sequences cause oncogene overexpression when the virus integrates near an oncogene. In this study, FGF3 is overexpressed. FGF3 binds to FGFR1 and regulates STAT3 and Akt phosphorylation as well as the expression of cyclin D1, c-myc, and p21, which contributes to the development of SBC. Phosphorylated STAT3 promotes Akt phosphorylation and vice versa. Both phosphorylated STAT3 and Akt inhibit the expression of FGFR1.