宫颈癌（CC）是最常见和最有害的妇科癌症之一，它通过遗传和表观遗传改变而演变，导致致癌活性的促进和肿瘤抑制机制的功能障碍。尽管医学取得了进步，但由于高复发率和对现有治疗的耐药性，晚期患者的预后仍然极低。因此，加强了对潜在预后生物标志物的探索，以揭示 CC 发病机制的新模式并开发新的抗癌疗法。表观转录组修饰，即可逆表观遗传 RNA 修饰，通过决定 RNA 命运以介导 RNA 相互作用来调节各种生物过程。这篇叙述性综述深入了解了内源性 RNA 编辑蛋白及其相关的表观转录组修饰，尤其是 N6-甲基腺苷 (m6A)、5-甲基胞嘧啶 (m5C) 和 N1-甲基腺苷 (m1A) 在控制发育中的细胞和分子作用， CC的进展和转移。我们讨论了 50 多种 RNA 调控的深入表观转录组机制，这些 RNA 负责肿瘤发生、增殖、迁移、侵袭、生存、自噬、干性、上皮-间质转化、代谢（葡萄糖、脂质、谷氨酸和谷氨酰胺）、耐药性（药物）和放射）、血管生成和 CC 复发。此外，我们还简要概述了针对 CC 中内源性 RNA 编辑蛋白表达改变和 RNA 修饰在编码和非编码 RNA 上的异常沉积的治疗潜力。

Cervical cancer (CC), one of the most prevalent and detrimental gynaecologic cancers, evolves through genetic and epigenetic alterations resulting in the promotion of oncogenic activity and dysfunction of tumour-suppressing mechanisms. Despite medical advancement, the prognosis for advanced-stage patients remains extremely low due to high recurrence rates and resistance to existing treatments. Thereby, the search for potential prognostic biomarkers is heightened to unravel new modalities of CC pathogenesis and to develop novel anti-cancer therapies. Epitranscriptomic modifications, reversible epigenetic RNA modifications, regulate various biological processes by deciding RNA fate to mediating RNA interactions. This narrative review provides insight into the cellular and molecular roles of endogenous RNA-editing proteins and their associated epitranscriptomic modifications, especially N6-methyladenosine (m6A), 5-methylcytosine (m5C) and N1-methyladenosine (m1A), in governing the development, progression and metastasis of CC. We discussed the in-depth epitranscriptomic mechanisms underlying the regulation of over 50 RNAs responsible for tumorigenesis, proliferation, migration, invasion, survival, autophagy, stemness, epithelial-mesenchymal transition, metabolism (glucose, lipid, glutamate and glutamine), resistance (drug and radiation), angiogenesis and recurrence of CC. Additionally, we provided a concise overview of the therapeutic potential of targeting the altered expression of endogenous RNA-editing proteins and aberrant deposition of RNA modifications on both coding and non-coding RNAs in CC.