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Updated: Sep 14, 2025

Clinicopathological Analysis of miRNA Expression in Breast Cancer Tissues by Using miRNA In Situ Hybridization
Published on: June 7, 2016
The circDUSP1/miR-429/DLC1 regulatory network affects proliferation, migration, and invasion of triple-negative
Canhui Jian1,2, Xiaoxue Tian1,2, Shuai Luo1
1Department of Pathology, Affiliated Hospital of Zunyi Medical University, Zunyi, 563003, Guizhou Province, China.
Abstract:
Triple-negative breast cancer (TNBC) is an aggressive subtype lacking effective targeted therapies, with circular RNAs (circRNAs) emerging as key regulators in cancer progression through competitive endogenous RNA (ceRNA) networks. Although circRNAs function as miRNA sponges in TNBC, the specific role of circDUSP1 in the miR-429/DLC1 pathway remains unknown. In this study, a circular RNA, circDUSP1, was identified as differentially expressed in TNBC using an online database. Using TNBC patient tissues and cell lines (MDA-MB-231/MDA-MB-468), we quantified circDUSP1 expression via qRT-PCR. The molecular characteristics of circDUSP1 were identified through methods such as nuclear-cytoplasmic separation, RNase R digestion, and FISH. Assessed the impact of circDUSP1 on TNBC cell proliferation/migration/invasion through functional assays (CCK-8, colony formation, Transwell, etc.). The circDUSP1/miR-429/DLC1 regulatory network's role in TNBC was validated using dual-luciferase reporter gene, RNA pull-down, and rescue assays. circDUSP1 was significantly downregulated in TNBC tissues and cell lines. circDUSP1 overexpression suppressed TNBC cell proliferation, migration, invasion, and tumor growth in vivo circDUSP1 directly bound miR-429 to relieve its repression of tumor suppressor DLC1 miR-429 mimics attenuated circDUSP1-mediated tumor suppression. circDUSP1 inhibits TNBC progression by acting as a molecular sponge for miR-429 to upregulate DLC1. This regulatory network represents a novel therapeutic target for TNBC.
Insights
Circular RNA circDUSP1 acts as a tumor suppressor in triple-negative breast cancer (TNBC). Overexpressing circDUSP1 inhibits TNBC cell growth and metastasis by sponging miR-429, thereby upregulating the DLC1 tumor suppressor.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Triple-negative breast cancer (TNBC) is aggressive and lacks targeted therapies.
- Circular RNAs (circRNAs) regulate cancer via competitive endogenous RNA (ceRNA) networks.
- The role of circDUSP1 in TNBC's miR-429/DLC1 pathway is unexplored.
Purpose of the Study:
- Investigate circDUSP1's expression and function in TNBC.
- Elucidate the circDUSP1/miR-429/DLC1 regulatory network in TNBC.
- Evaluate circDUSP1 as a potential therapeutic target for TNBC.
Main Methods:
- Bioinformatic analysis, qRT-PCR, and patient tissue/cell line analysis.
- Molecular characterization (nuclear-cytoplasmic separation, RNase R, FISH).
- Functional assays (proliferation, migration, invasion, in vivo tumor growth), dual-luciferase, RNA pull-down, and rescue assays.
Main Results:
- circDUSP1 was significantly downregulated in TNBC tissues and cell lines.
- circDUSP1 overexpression suppressed TNBC cell proliferation, migration, invasion, and tumor growth.
- circDUSP1 directly bound miR-429, relieving miR-429's repression of DLC1.
Conclusions:
- circDUSP1 functions as a tumor suppressor in TNBC.
- circDUSP1 inhibits TNBC progression by upregulating DLC1 via sponging miR-429.
- The circDUSP1/miR-429/DLC1 axis is a novel therapeutic target for TNBC.
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