ArticleCancer cell international2026
Characterization of Circ_0048766: an oncogenic circular rna promoting triple-negative breast cancer progression via the miR-329-3p/CXCR4 axis and regulated by METTL3.
Article in Cancer cell international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundCircular_RNAs (circ_RNAs) are involved in the development and progression of human malignancies, including breast cancer. Novel circ_RNAs for breast cancer remain to be further determined. This study investigates the role and mechanism of a novel circ_RNA circ_0048766 in triple-negative breast cancer (TNBC) progression.
methodsBioinformatics analysis was performed using the GSE165884 database to identify differentially expressed circ_RNAs. The expression of circ_0048766 was validated in various breast cancer cell lines through quantitative real-time PCR. Functional assays, including CCK-8, flow cytometry, colony formation, and Transwell assays, were conducted in BT-549 and MDA-MB-231 cells. The mechanisms involving methyltransferase-like 3 (METTL3), miR-329-3p, and C-X-C Motif Chemokine Receptor 4 (CXCR4) were examined through bioinformatics, dual-luciferase reporter assays, RNA immunoprecipitation, and RNA pull-down. In vivo studies were conducted using a nude mouse xenograft model to evaluate tumor growth and CXCR4 expression.
resultsCirc_0048766 was significantly upregulated in TNBC cell lines compared to normal breast epithelial cells. Knockdown of circ_0048766 resulted in reduced cell viability, colony formation, migration, and invasion while increasing apoptosis in BT-549 and MDA-MB-231 cells. Mechanistically, circ_0048766 was confirmed to function as a sponge for miR-329-3p. Moreover, miR-329-3p directly suppressed CXCR4 expression, and circ_0048766 regulated CXCR4 in a miR-329-3p-dependent manner. Additionally, circ_0048766 promoted epithelial-mesenchymal transition, as evidenced by its regulation of E-cadherin, N-cadherin, and Vimentin expression via miR-329-3p. MiR-329-3p inhibition or CXCR4 overexpression reversed the effects of circ_0048766 knockdown. In vivo, circ_0048766 knockdown significantly diminished tumor growth and weight, along with decreased CXCR4 levels. METTL3 was identified as an upstream regulator mediating m6A modification of circ_0048766. Functionally, METTL3 knockdown suppressed CXCR4 expression and cell proliferation, effects that were rescued by CXCR4 overexpression.
conclusionsCirc_0048766 is a novel oncogenic circ_RNA that promotes TNBC progression through the miR-329-3p/CXCR4 signaling axis, regulated by METTL3. This study highlights the potential of targeting the METTL3/circ_0048766/miR-329-3p/CXCR4 axis as a novel therapeutic strategy for TNBC treatment.
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