KEY TAKEAWAYS
- The study aimed to explore hsa_circ_0003528’s role and impact in TNBC to understand its functional significance.
- Researchers noticed that hsa_circ_003528 promotes aggressive TNBC behaviors via miR-215, highlighting its potential as a biomarker and therapeutic target.
Among breast cancer subtypes, triple-negative breast cancer (TNBC) is noted for its high malignancy and poor prognosis. Understanding the molecular mechanisms driving TNBC is crucial due to its aggressive nature.
Ru Chang and the team aimed to investigate the expression and functional role of hsa_circ_0003528, specifically in TNBC, and its potential impact on the disease.
Researchers evaluated hsa_circ_0003528 expression changes using the GEO database (GSE101123) and confirmed them with RT-qPCR. They assessed the clinical significance through χ2 tests and Kaplan-Meier curves. They used bioinformatics and dual-luciferase reporter assays to find potential miRNAs affected by hsa_circ_0003528. Cellular experiments were then performed to see how hsa_circ_0003528 and/or miR-215 influence TNBC cells.
The hsa_circ_003528 was identified from the circRNA profile in the GSE101123 dataset, showing higher expression in breast cancer, especially in TNBC tissues. Increased levels of hsa_circ_003528 were linked to poorer overall survival (OS) in patients with TNBC. Silencing hsa_circ_003528 induced TNBC cell proliferation, migration, and invasion. However, reducing miR-215 partially lessened the effects of hsa_circ_003528 silencing on these TNBC cells.
The study concluded that hsa_circ_0003528 is upregulated in TNBC, promoting aggressive cellular behaviors through miR-215 regulation. This indicates its potential as a valuable biomarker and therapeutic target for TNBC treatment.
The study received no funds.
Source: https://pubmed.ncbi.nlm.nih.gov/39126511/
Chang R, Yu H, Li S, et al. (2024). “CircRNA hsa_circ_0003528/miR-215 is considered a potential target for predictive prognosis and therapy for triple-negative breast cancer.” Mol Biol Rep. 2024 Aug 10;51(1):901. doi: 10.1007/s11033-024-09808-8. PMID: 39126511.
