Impact of microRNA variants on PI3K/AKT signaling in triple-negative breast cancer: comprehensive review

• Published in: Medical oncology (Northwood, London, England) London, England), 2024-08, Vol.41 (9), p.222, Article 222
• Main Authors: Mehrtabar, Ehsan, Khalaji, Amirreza, Pandeh, Mojtaba, Farhoudian, Aram, Shafiee, Nadia, Shafiee, Atefe, Ojaghlou, Fatemeh, Mahdavi, Parinaz, Soleymani-Goloujeh, Mehdi
• Format: Article
• Language: English
• Subjects: Breast cancer; Female; Gene Expression Regulation, Neoplastic; Hematology; Humans; Internal Medicine; Medicine; Medicine & Public Health; MicroRNAs; MicroRNAs - genetics; Oncology; Pathology; Phosphatidylinositol 3-Kinases - genetics; Phosphatidylinositol 3-Kinases - metabolism; Proto-Oncogene Proteins c-akt - genetics; Proto-Oncogene Proteins c-akt - metabolism; Review; Signal Transduction - genetics; Triple Negative Breast Neoplasms - genetics; Triple Negative Breast Neoplasms - metabolism; Triple Negative Breast Neoplasms - pathology
• ISSN: 1559-131X; 1357-0560; 1559-131X
• DOI: 10.1007/s12032-024-02469-4

Breast cancer (BC) is a significant cause of cancer-related mortality, and triple-negative breast cancer (TNBC) is a particularly aggressive subtype associated with high mortality rates, especially among younger females. TNBC poses a considerable clinical challenge due to its aggressive tumor behavior and limited therapeutic options. Aberrations within the PI3K/AKT pathway are prevalent in TNBC and correlate with increased therapeutic intervention resistance and poor outcomes. MicroRNAs (miRs) have emerged as crucial PI3K/AKT pathway regulators influencing various cellular processes involved in TNBC pathogenesis. The levels of miRs, including miR-193, miR-4649-5p, and miR-449a, undergo notable changes in TNBC tumor tissues, emphasizing their significance in cancer biology. This review explored the intricate interplay between miR variants and PI3K/AKT signaling in TNBC. The review focused on the molecular mechanisms underlying miR-mediated dysregulation of this pathway and highlighted specific miRs and their targets. In addition, we explore the clinical implications of miR dysregulation in TNBC, particularly its correlation with TNBC prognosis and therapeutic resistance. Elucidating the roles of miRs in modulating the PI3K/AKT signaling pathway will enhance our understanding of TNBC biology and unveil potential therapeutic targets. This comprehensive review aims to discuss current knowledge and open promising avenues for future research, ultimately facilitating the development of precise and effective treatments for patients with TNBC.