ArticleFunctional & integrative genomics2024
RUNX3 exerts tumor-suppressive role through inhibiting EXOSC4 expression.
Article in Functional & integrative genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Upregulation of the Mitophagy-Related Gene EXOSC4 Is Associated with Immune Dysregulation in Spinal Cord Injury.Molecular neurobiology · 2026Article
- Decoding the enhancer-driven regulatory network for lactoferrin across mammalian species.Zoological research · 2026Article
- EXOSC4 as a novel regulator of neddylation in acute myeloid leukemia.Scientific reports · 2026Article
- Ribosomal Protein RPL29 Promotes Hepatocellular Carcinoma Progression Through Regulation the Expression of Exosome Component 4.Biological procedures online · 2026Article
- ETS Homologous Factor (EHF) and Gamma Linolenic Acid (GLA): novel strategies for early diagnosis and treatment of endometriosis.Functional & integrative genomics · 2026Article
- miR-495 suppresses osteosarcoma growth and metastasis by directly targeting RUNX3 in the PI3K/Akt pathwayFrontiers in cell and developmental biology · 2026Article
- Construction of a prognostic risk model for acute myeloid leukemia based on exosomal genes and analysis of immune microenvironment characteristics.Scientific reports · 2025Article
- Identification EXOSC4 as a novel autoantigen of interstitial lung disease in rheumatoid arthritis.Journal of translational medicine · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.