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 1;13(9):754. doi: 10.1038/s41419-022-05182-0

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

© The Author(s) 2022

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

Fig. 8 — In PCa, ivermectin could target FOXA1 and Ku70/Ku80. The interaction of ivermectin and FOXA1 reduced the chromatin accessibility of AR signaling and E2F1, leading to cell cycle arrest and inhibiting cell proliferation. The interaction of ivermectin and Ku70/Ku80 block the recruitment of Ku70/Ku80 to DSB sites. Cooperating with the downregulation of AR regulated homologous recombination repair genes, BRCA1 and Rad51, ivermectin increased intracellular DNA damage level and triggered synthetic lethality.