Unraveling the Role of the microRNA-Mediated Regulation of Actin-Binding Proteins in Ovarian Cancer: A Narrative Review

Abstract

Ovarian cancer remains one of the most lethal gynecological malignancies, primarily due to its late diagnosis and limited prospects for successful treatment. MiRNAs have been shown to be important post-transcriptional regulators in a variety of cancer-related pathways in recent years. One of the principal mechanisms underlying the motility, invasiveness, and metastatic potential of ovarian cancer cells is the microRNA-mediated regulation of ABPs. As integral components of the cytoskeletal network, ABPs participate in dynamic cellular processes such as migration, adhesion, and invasion, and are critically involved in tumor development and progression. Recent data indicate that some miRNAs affect ABP expression and activity, which in turn affects cytoskeletal remodeling and, ultimately, tumor cell behavior. The role of miRNAs in cancer development is inherently complex due to their ability to function as both tumor suppressors and oncogenes, depending on the molecular context. Key ABPs that are targeted by particular miRNAs are discussed in terms of their clinical relevance, including their potential utility as diagnostic biomarkers or therapeutic targets. A deeper understanding of these regulatory pathways may offer new opportunities for early detection and personalized treatment strategies. In this narrative review, the current knowledge of how miRNAs affect ABP expression and function, and how this interaction contributes to the development and progression of ovarian cancer, is compiled.

Keywords: actin-binding proteins; biomarker; cytoskeleton; gene regulation; microRNA (miRNA); ovarian cancer.

Figure 1

Schematic overview of microRNA-mediated regulation of gene expression. Mature miRNAs are loaded into the RNA-induced silencing complex (RISC), where they guide the complex to complementary sequences in the 3′ untranslated regions (3′ UTRs) of target mRNAs. This interaction results in translational repression and/or mRNA degradation, ultimately leading to reduced protein output. Ago2: Argonaute 2, TDMD: target-directed miRNA degradation.