Perspectives on OncomiR and TSmiRs in Breast Cancer and Assessment of their Regulatory Network
Breast cancer stands as a primary cause of mortality among women, urging the exploration of novel avenues for early detection. MicroRNAs (miRNAs) emerge as promising biomarkers, acting as both oncogenes and tumor suppressors, thus offering the potential for breakthroughs in early detection. Elevated levels of oncogenic miRNAs (OncomiRs) in cancer foster cell proliferation, migration, and metastasis by suppressing tumor suppressor genes. Inhibiting OncomiRs function presents a promising treatment strategy, where synthetic anti-miRs hinder OncomiRs binding to target RNAs, effectively suppressing cancer cell growth and metastasis. Conversely, decreased expression of Tumor Suppressor miRNAs (TSmiRs) in cancer facilitates malignancy progression by failing to suppress cancer-promoting genes. Circulating microRNAs (miRNAs) have gained considerable interest as promising biomarkers for breast cancer, owing to their distinct properties and involvement in cancer progression. An essential benefit of circulating miRNAs is their presence in bodily fluids like blood, serum, plasma, and breast milk. They exhibit remarkable stability within these fluids, safeguarded against degradation through encapsulation within extracellular vesicles or binding with proteins. This stability renders them appealing candidates for non-invasive biomarker identification. This article provides an overview of miRNA’s pivotal role in breast cancer and its clinical significance. Keywords breast cancer, non-invasive, biomarker, miRNA, serum, prognosis
Authors
- Jemmy Christy (ORCID: https://orcid.org/0000-0002-5538-4270)
- Grace Lydia Phoebe
Institutions
- Sathyabama Institute of Science and Technology (IN)
Publication Details
- Journal
- Biomedical Sciences and Clinical Medicine
- Published
- 2024-10-01
- DOI
- https://doi.org/10.12982/bscm.2024.32
- Primary Topic
- Advanced Biosensing Techniques and Applications
- Type
- article
- Field-Weighted Citation Impact
- 0.00