Cervical cancer (CC) is a significant health issue, particularly in low-income countries, primarily caused by persistent infection with high-risk human papillomavirus (HPV) types. While HPV is responsible for nearly all CC cases, some cases are HPV-negative, often being adenocarcinomas. Over 200 HPV types exist, with 15 classified as high-risk, including HPV16, which is found in about 60% of CC cases. HPV is a small, non-enveloped virus with a circular DNA genome that can integrate into the host genome, contributing to CC development. The integration of HPV into the host genome is associated with the progression of cervical lesions, and the expression of viral oncoproteins E5, E6, and E7 plays a critical role in the development of CC by modulating cell proliferation, immune evasion, apoptosis, and genomic instability. E5 affects signaling pathways involved in interferon-induced genes and EGFR-induced proliferation, while E6 and E7 regulate DNA repair and cell cycle continuity. Next-generation technologies have provided extensive information on molecular changes in CC, including genome, transcriptome, proteome, metabolome, and epigenome, leading to the identification of novel molecular traits as potential biomarkers and therapeutic targets. The study highlights the importance of understanding the molecular mechanisms of HPV oncogenesis and the role of various signaling pathways in CC progression. It also emphasizes the significance of the host's immune response in controlling HPV infection and the impact of the cervical microbiome on CC development. The research underscores the need for further investigation into the molecular mechanisms of CC and the development of targeted therapies based on these findings.Cervical cancer (CC) is a significant health issue, particularly in low-income countries, primarily caused by persistent infection with high-risk human papillomavirus (HPV) types. While HPV is responsible for nearly all CC cases, some cases are HPV-negative, often being adenocarcinomas. Over 200 HPV types exist, with 15 classified as high-risk, including HPV16, which is found in about 60% of CC cases. HPV is a small, non-enveloped virus with a circular DNA genome that can integrate into the host genome, contributing to CC development. The integration of HPV into the host genome is associated with the progression of cervical lesions, and the expression of viral oncoproteins E5, E6, and E7 plays a critical role in the development of CC by modulating cell proliferation, immune evasion, apoptosis, and genomic instability. E5 affects signaling pathways involved in interferon-induced genes and EGFR-induced proliferation, while E6 and E7 regulate DNA repair and cell cycle continuity. Next-generation technologies have provided extensive information on molecular changes in CC, including genome, transcriptome, proteome, metabolome, and epigenome, leading to the identification of novel molecular traits as potential biomarkers and therapeutic targets. The study highlights the importance of understanding the molecular mechanisms of HPV oncogenesis and the role of various signaling pathways in CC progression. It also emphasizes the significance of the host's immune response in controlling HPV infection and the impact of the cervical microbiome on CC development. The research underscores the need for further investigation into the molecular mechanisms of CC and the development of targeted therapies based on these findings.