The circDUSP1/miR-429/DLC1 regulatory network affects proliferation, migration, and invasion of triple-negative breast cancer cells

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.