RUNX3 exerts tumor-suppressive role through inhibiting EXOSC4 expression.


Journal

Functional & integrative genomics
ISSN: 1438-7948
Titre abrégé: Funct Integr Genomics
Pays: Germany
ID NLM: 100939343

Informations de publication

Date de publication:
17 May 2024
Historique:
received: 24 02 2024
accepted: 01 05 2024
revised: 23 04 2024
medline: 24 6 2024
pubmed: 24 6 2024
entrez: 24 6 2024
Statut: epublish

Résumé

Breast cancer severely affects women health. 70% of breast cancer are estrogen receptor positive. Breast cancer stem cells are a group of tumor with plasticity, causing tumor relapse and metastasis. RUNX3 is a tumor suppressor frequently inactivated in estrogen receptor positive breast cancer. However, the mechanism of how RUNX3 is involved in the regualation of cancer stem cell traits in estrogen receptor positive breast cancer remains elusive. In this study, we utilized cut-tag assay to investigate the binding profile RUNX3 in BT474 and T47D cell, and confirmed EXOSC4 as the bona-fide target of RUNX3; RUNX3 could bind to the promoter are of EXOSC4 to suppress its expression. Furthermore, EXOSC4 could increase the colony formation, cell invasion and mammosphere formation ability of breast cancer cells and upregulate the the expression of SOX2 and ALDH1. Consistent with these findings, EXOSC4 was associated with poorer survival for Luminal B/Her2 breast cancer patiens. At last, we confirmed that EXOSC4 mediated the tumor suppressive role of RUNX3 in breast cancer cells. In conclusion, we demonstrate that RUNX3 directly binds to the promoter region of EXOSC4, leading to the suppression of EXOSC4 expression and exerting a tumor-suppressive effect in estrogen receptor postivive breast cancer cells.

Identifiants

pubmed: 38913281
doi: 10.1007/s10142-024-01363-6
pii: 10.1007/s10142-024-01363-6
doi:

Substances chimiques

Core Binding Factor Alpha 3 Subunit 0
Runx3 protein, human 0
Aldehyde Dehydrogenase 1 Family EC 1.2.1
SOXB1 Transcription Factors 0
ALDH1A1 protein, human EC 1.2.1.36
Retinal Dehydrogenase EC 1.2.1.36
SOX2 protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

103

Subventions

Organisme : National Natural Science Foundation of China
ID : No. 82003165
Organisme : National Natural Science Foundation of China
ID : No. 82003165
Organisme : National Natural Science Foundation of China
ID : No. 82003165
Organisme : National Natural Science Foundation of China
ID : No. 82003165
Organisme : National Natural Science Foundation of China
ID : No. 82003165
Organisme : National Natural Science Foundation of China
ID : No. 82003165
Organisme : National Natural Science Foundation of China
ID : No. 82003165
Organisme : National Natural Science Foundation of China
ID : No. 82003165

Informations de copyright

© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

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Auteurs

Nan Wang (N)

Department of Pathology, Xuzhou Medical University, Xuzhou, China.

Xiaodan Miao (X)

Department of Pathology, Xuzhou Medical University, Xuzhou, China.

Wenxin Lu (W)

Department of Pathology, Xuzhou Medical University, Xuzhou, China.

Yang Ji (Y)

Department of Pathology, Xuzhou Medical University, Xuzhou, China.

Yuxin Zheng (Y)

Department of Pathology, Xuzhou Medical University, Xuzhou, China.

Di Meng (D)

Department of Pathology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.

Hui Liu (H)

Department of Pathology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
Department of Pathology, Xuzhou Medical University, Xuzhou, China.

Chenxi Xiang (C)

Department of Pathology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China. hejubu@foxmail.com.
Department of Pathology, Xuzhou Medical University, Xuzhou, China. hejubu@foxmail.com.

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