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

. 2022 Sep 20;22:289. doi: 10.1186/s12935-022-02713-9

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

© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

PMC Copyright notice

Fig. 7 — Hypothetical overview of multiple actions of β-escin on cancer stem-like features, HER2/HER3/Akt pathway and trastuzumab resistance within HER2-positive breast cancer. β-escin exerts antitumor activity via the intrinsic mitochondrial apoptotic pathway and suppression of cancer stem-like properties including CD44^high/CD24^low stem-like population and ALDH1 activity. Mitochondrial-mediated apoptosis was accompanied by elevated oxidative stress and a marked increase in active p18Bax fragment levels, leading to the release of cytochrome c as well as consequent activation of caspase-3 and caspase-7. β-escin impairs the HER2/HER3/Akt pathway coinciding with downregulation of truncated-p95HER2 in HER2-positive breast cancer cells that are both trastuzumab-sensitive and –resistant