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 Oct 3;12:1024600. doi: 10.3389/fonc.2022.1024600

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

Copyright © 2022 Takayama and Inoue

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

Enhanced phase-separation by transcription factor collaborations for prostate cancer progression. (A) OCT4 promotes TF complex formation by enhancing LLPS in PC specific SE regions. In AR positive PC cells, OCT4 interacts with AR, FOXA1 and activates SEs to induce important genes for PC progression. (B) Disease specific TF collaboration for PC progression. In AR positive PC cells, OCT4/FOXA1/AR complex regulates genes associated with tumor growth and pluripotency. Repression of AR is frequently observed in NEPC characterized by an aggressive clinical course. In AR negative CRPC cells, OCT4 forms a complex with NRF1 to induce specific target genes associated with DNA damage response for chemotherapy-resistance.