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 Jun 30;13:909821. doi: 10.3389/fphar.2022.909821

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

Copyright © 2022 Liu, Zhang, Wu, Xu, Ma, Wu and Xia.

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

Ferroptosis and cancer metastasis. (1) Various changes in the E-cadherin-Merlin-Hippo-YAP axis are associated with ferroptosis. When E-cadherin, Merlin, and Hippo are inhibited, YAP is activated to further induce ferroptosis, while NF2/Merlin Deficiency drives cancer metastasis. (2) EMT is favorable to the survival of cancer cells and metastasis, which blocks E-cadherin-induced cell–cell interactions and activates YAP, thus leading to ferroptosis. MTDH contributes to ferroptosis by reducing intracellular GSH levels by downregulating GPX4 and SLC3A2. (3) HIF has a dual role in regulating ferroptosis in cancer cells. Activated HIF-2α upregulates lipid and iron-regulated genes and enhances lipid peroxidation of PUFAs, thus enhancing their sensitivity to ferroptosis. In contrast, it prevents ferroptosis in cancer cells by improving the cellular uptake of fatty acids and lipid storage by upregulating FABP3 and FABP7.