HPV-Driven Pathways and Genetic Determinants of Cervical Cancer Susceptibility: A Comprehensive Analysis

Cervical cancer is a significant public health issue, especially in low- and middle-income countries, where access to HPV screening and vaccination is limited. Persistent infection with high-risk Human papillomavirus (HPV) variants is the primary cause of cervical cancer. HPV oncoproteins E5, E6, and E7 interact with host cellular components, promoting oncogenesis through key signaling pathways, including PI3K/Akt, Wnt/β-catenin, ERK/MAPK, and JAK/STAT. This review examines the role of long non-coding RNAs (lncRNAs) and their associated single-nucleotide polymorphism (SNPs) in cervical cancer development. It also explores the association of HPV with various cellular pathways contributing to cancer progression. Specifically, the review focuses on SNPs in lncRNAs H19, HOTAIR, HOTTIP, and CASC8, as well as ANRIL and MALAT1, and their potential as biomarkers for cervical cancer susceptibility in the Chinese Han population. The review compiles findings from recent studies investigating the association of specific SNPs (e.g., rs217727, rs2366152, rs1859168, rs10505477) in lncRNAs with cervical cancer risk. It evaluates data from genomic analyses of case-control studies to understand the functional impact of these polymorphisms on cancer-related pathways. Significant associations were identified between specific SNPs in lncRNAs within cancer pathways, highlighting their role in disease progression. LncRNA polymorphisms and their interaction with HPV-associated pathways may serve as valuable biomarkers for early detection and risk assessment of cervical cancer. Further research is essential to validate these findings and explore their therapeutic potential.