CREPT is required for the metastasis of triple-negative breast cancer through a co-operational-chromatin loop-based gene regulation

Abstract Triple-negative breast cancer (TNBC) is recognized for its aggressiveness, yet the mechanism underlying metastasis remains unclear. Here, we report that CREPT/RPRD1B, which exhibits somatic gene copy-number amplifications and elevated expression, correlates with poor patient survival and dr...

Full description

Saved in:
Bibliographic Details
Main Authors: Jianghua Li, Lu Xu, Jiayu Wang, Xuning Wang, Yuting Lin, Alex Yutian Zou, Fangli Ren, Yinyin Wang, Jun Li, Zhijie Chang
Format: Article
Language:English
Published: BMC 2025-06-01
Series:Molecular Cancer
Online Access:https://doi.org/10.1186/s12943-025-02361-3
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849691412169228288
author Jianghua Li
Lu Xu
Jiayu Wang
Xuning Wang
Yuting Lin
Alex Yutian Zou
Fangli Ren
Yinyin Wang
Jun Li
Zhijie Chang
author_facet Jianghua Li
Lu Xu
Jiayu Wang
Xuning Wang
Yuting Lin
Alex Yutian Zou
Fangli Ren
Yinyin Wang
Jun Li
Zhijie Chang
author_sort Jianghua Li
collection DOAJ
description Abstract Triple-negative breast cancer (TNBC) is recognized for its aggressiveness, yet the mechanism underlying metastasis remains unclear. Here, we report that CREPT/RPRD1B, which exhibits somatic gene copy-number amplifications and elevated expression, correlates with poor patient survival and drives TNBC metastasis. We demonstrate that CREPT alters three-dimensional genome structures in topologically-associating domain (TAD) status and chromatin loops via occupying promoters and enhancers. Specifically, CREPT mediates 1082 co-operational chromatin loops configured by enhancer-promoter and promoter-termination loops, which are validated by HiChIP analyses and visualized by Tn5-FISH experiments. These loops orchestrate RNAPII loading and recycling to enhance the metastatic gene expression. Disruption of these co-operational loops using CRISPR-dCas9 suppresses TNBC metastasis in vivo. Furthermore, depletion of CREPT using an AAV-based shRNA blocks TNBC metastasis in both preventative and therapeutic mouse models. We propose that targeting CREPT to disrupt the co-operational chromatin loop structures represents a promising therapeutic strategy for metastatic TNBC. Graphical Abstract
format Article
id doaj-art-cd1a2e2630144250a17df470fc276e58
institution DOAJ
issn 1476-4598
language English
publishDate 2025-06-01
publisher BMC
record_format Article
series Molecular Cancer
spelling doaj-art-cd1a2e2630144250a17df470fc276e582025-08-20T03:21:02ZengBMCMolecular Cancer1476-45982025-06-0124114010.1186/s12943-025-02361-3CREPT is required for the metastasis of triple-negative breast cancer through a co-operational-chromatin loop-based gene regulationJianghua Li0Lu Xu1Jiayu Wang2Xuning Wang3Yuting Lin4Alex Yutian Zou5Fangli Ren6Yinyin Wang7Jun Li8Zhijie Chang9State Key Laboratory of Membrane Biology, School of Basic Medical Sciences, School of Medicine, Tsinghua UniversityState Key Laboratory of Membrane Biology, School of Basic Medical Sciences, School of Medicine, Tsinghua UniversityState Key Laboratory of Membrane Biology, School of Basic Medical Sciences, School of Medicine, Tsinghua UniversityDepartment of General Surgery, General Hospital of Northern Theater CommandState Key Laboratory of Membrane Biology, School of Basic Medical Sciences, School of Medicine, Tsinghua UniversityCollege of Letters & Science, University of California BerkeleyState Key Laboratory of Membrane Biology, School of Basic Medical Sciences, School of Medicine, Tsinghua UniversityState Key Laboratory of Membrane Biology, School of Basic Medical Sciences, School of Medicine, Tsinghua UniversityJinfeng LaboratoryState Key Laboratory of Membrane Biology, School of Basic Medical Sciences, School of Medicine, Tsinghua UniversityAbstract Triple-negative breast cancer (TNBC) is recognized for its aggressiveness, yet the mechanism underlying metastasis remains unclear. Here, we report that CREPT/RPRD1B, which exhibits somatic gene copy-number amplifications and elevated expression, correlates with poor patient survival and drives TNBC metastasis. We demonstrate that CREPT alters three-dimensional genome structures in topologically-associating domain (TAD) status and chromatin loops via occupying promoters and enhancers. Specifically, CREPT mediates 1082 co-operational chromatin loops configured by enhancer-promoter and promoter-termination loops, which are validated by HiChIP analyses and visualized by Tn5-FISH experiments. These loops orchestrate RNAPII loading and recycling to enhance the metastatic gene expression. Disruption of these co-operational loops using CRISPR-dCas9 suppresses TNBC metastasis in vivo. Furthermore, depletion of CREPT using an AAV-based shRNA blocks TNBC metastasis in both preventative and therapeutic mouse models. We propose that targeting CREPT to disrupt the co-operational chromatin loop structures represents a promising therapeutic strategy for metastatic TNBC. Graphical Abstracthttps://doi.org/10.1186/s12943-025-02361-3
spellingShingle Jianghua Li
Lu Xu
Jiayu Wang
Xuning Wang
Yuting Lin
Alex Yutian Zou
Fangli Ren
Yinyin Wang
Jun Li
Zhijie Chang
CREPT is required for the metastasis of triple-negative breast cancer through a co-operational-chromatin loop-based gene regulation
Molecular Cancer
title CREPT is required for the metastasis of triple-negative breast cancer through a co-operational-chromatin loop-based gene regulation
title_full CREPT is required for the metastasis of triple-negative breast cancer through a co-operational-chromatin loop-based gene regulation
title_fullStr CREPT is required for the metastasis of triple-negative breast cancer through a co-operational-chromatin loop-based gene regulation
title_full_unstemmed CREPT is required for the metastasis of triple-negative breast cancer through a co-operational-chromatin loop-based gene regulation
title_short CREPT is required for the metastasis of triple-negative breast cancer through a co-operational-chromatin loop-based gene regulation
title_sort crept is required for the metastasis of triple negative breast cancer through a co operational chromatin loop based gene regulation
url https://doi.org/10.1186/s12943-025-02361-3
work_keys_str_mv AT jianghuali creptisrequiredforthemetastasisoftriplenegativebreastcancerthroughacooperationalchromatinloopbasedgeneregulation
AT luxu creptisrequiredforthemetastasisoftriplenegativebreastcancerthroughacooperationalchromatinloopbasedgeneregulation
AT jiayuwang creptisrequiredforthemetastasisoftriplenegativebreastcancerthroughacooperationalchromatinloopbasedgeneregulation
AT xuningwang creptisrequiredforthemetastasisoftriplenegativebreastcancerthroughacooperationalchromatinloopbasedgeneregulation
AT yutinglin creptisrequiredforthemetastasisoftriplenegativebreastcancerthroughacooperationalchromatinloopbasedgeneregulation
AT alexyutianzou creptisrequiredforthemetastasisoftriplenegativebreastcancerthroughacooperationalchromatinloopbasedgeneregulation
AT fangliren creptisrequiredforthemetastasisoftriplenegativebreastcancerthroughacooperationalchromatinloopbasedgeneregulation
AT yinyinwang creptisrequiredforthemetastasisoftriplenegativebreastcancerthroughacooperationalchromatinloopbasedgeneregulation
AT junli creptisrequiredforthemetastasisoftriplenegativebreastcancerthroughacooperationalchromatinloopbasedgeneregulation
AT zhijiechang creptisrequiredforthemetastasisoftriplenegativebreastcancerthroughacooperationalchromatinloopbasedgeneregulation