Cervical cancer remains a significant global health concern, impacting over half a million women annually. The primary cause is a persistent infection with hr-HPV, which disrupts various cellular processes crucial for normal function. This disruption leads to genetic instability, including changes in the expression of microRNAs and their corresponding host genes, with far-reaching consequences for cellular regulation. Researchers have widely utilized high-throughput technologies to analyze gene expression in cervical cancer, aiming to identify distinct molecular signatures of microRNAs and genes through genomic analysis. However, discrepancies among studies have been noted, possibly due to variations in sample collection, technological platforms, and data processing methods such as normalization and filtering. Therefore, it is essential to synthesize findings from diverse studies to comprehensively understand the molecular mechanisms of regulatory genetic networks involved in the initiation and progression of cervical cancer. This review examined the evidence detailing the role of microRNA signatures and their target genes in cervical carcinogenesis and disease advancement. The accumulated data suggest the presence of widespread regulatory genetic networks active in both precancerous and cancerous cervical cells, potentially acting as key drivers of this malignancy. Identifying these molecular genomic signatures could open new avenues for developing therapeutic strategies for cervical cancer, particularly in the realm of precision medicine.

With an incidence of over a half million cases every year, cervical cancer remains a major health problem for women worldwide. Epidemiologic and molecular studies have clearly confirmed a causal role of persistent infection with high-risk human papillomavirus in cervical carcinogenesis, affecting several cellular processes. During cervical cancer development, there is genetic instability including disrupted expression of microRNAs and host target genes, which may have multiple implications. Different studies have explored the gene expression profile in cervical cancer using high-throughput technologies, with the goal of identifying microRNA and/or gene molecular signatures from genomics analysis of cervical cancer. However, the results of some studies have been divergent, which may be due to differences in sample collection procedures, high-throughput platforms, data normalization, and filtering methods used in different protocols. Hence, it is imperative to integrate information about diagnostic or prognostic biomarkers from a variety of sources to characterize the molecular mechanisms of regulatory genetic networks in cervical cancer development and progression. In the present review, we analyze the evidence that describes the role of microRNA signatures and target genes in cervical carcinogenesis and cancer progression. The data reviewed support the existence of universal regulatory genetic networks, which operate in cervical pre-cancerous and cancer cells and may represent the main driving forces in this malignancy. This analysis will allow molecular genomic signatures to be put forward as therapeutic targets for cervical cancer, with potential applications in precision medicine.