Background/Objectives: Thyroid cancer (TC) is the most common type of endocrine neoplasm and is increasing in incidence, particularly papillary thyroid carcinoma (PTC). Early-stage disease has a favorable prognosis; however, advanced forms, such as anaplastic thyroid carcinoma, complicate treatment. Long non-coding RNAs (lncRNAs), longer than 200 nucleotides and non-coding, together with microRNAs, have emerged as major regulators of TC pathogenesis. This review summarizes data on how dysregulated lncRNAs influence the hallmarks of cancer in thyroid malignancies.Methods: We reviewed the literature on the role of lncRNAs and microRNAs in TC, focusing on their functions as competing endogenous RNAs (ceRNAs), regulators of PI3K/AKT and Wnt/β-catenin pathways, and controllers of epigenetic alterations.Results: Dysregulated lncRNAs contribute to hallmarks including sustained growth, evading suppressors, resisting death, replicative immortality, angiogenesis, invasion, metabolic reprogramming, immune evasion, genomic instability, and tumor-promoting inflammation. ceRNA mechanisms amplify immune evasion by regulating checkpoint proteins and cytokines, altering immune cell activity. Altered lncRNA profiles correlate with aggressiveness, metastasis, and prognosis. Notable lncRNAs, such as H19, MALAT1, and DOCK9-AS2, dysregulate oncogenic pathways and represent potential biomarkers.Conclusions: Advances in therapeutics suggest inhibiting oncogenic lncRNAs or restoring tumor-suppressive lncRNAs via RNA interference, antisense oligonucleotides, or CRISPR/Cas9 editing. New technologies, including single-cell RNA sequencing and spatial transcriptomics, will improve understanding of heterogeneous lncRNA–microRNA networks in TC and support precision medicine. LncRNAs signify both molecular drivers and clinical targets for thyroid cancer.
背景/目的：甲状腺癌是最常见的内分泌系统肿瘤，其发病率呈上升趋势，其中以甲状腺乳头状癌尤为显著。早期甲状腺癌预后良好，但晚期类型如未分化甲状腺癌使治疗变得复杂。长度超过200个核苷酸的非编码长链RNA与微小RNA共同成为甲状腺癌发病机制的关键调控因子。本综述系统总结了异常表达的长链RNA如何影响甲状腺恶性肿瘤恶性特征的相关研究数据。 方法：我们回顾了关于长链RNA和微小RNA在甲状腺癌中作用的文献，重点关注其作为竞争性内源RNA的功能、对PI3K/AKT和Wnt/β-catenin通路的调控作用，以及对表观遗传改变的控制机制。 结果：异常表达的长链RNA参与调控包括持续增殖、逃避生长抑制、抵抗细胞死亡、复制永生、诱导血管生成、侵袭转移、代谢重编程、免疫逃逸、基因组不稳定和促肿瘤炎症在内的癌症特征。竞争性内源RNA机制通过调控检查点蛋白和细胞因子，改变免疫细胞活性，从而放大免疫逃逸效应。长链RNA表达谱的改变与肿瘤侵袭性、转移能力和预后密切相关。H19、MALAT1、DOCK9-AS2等关键长链RNA通过失调致癌通路发挥作用，展现出作为潜在生物标志物的价值。 结论：治疗学进展表明，通过RNA干扰、反义寡核苷酸或CRISPR/Cas9基因编辑技术抑制致癌性长链RNA或恢复抑癌性长链RNA功能具有可行性。单细胞RNA测序和空间转录组学等新技术将深化对甲状腺癌中异质性长链RNA-微小RNA网络的理解，为精准医疗提供支持。长链RNA既是甲状腺癌的分子驱动因子，也是潜在的临床治疗靶点。
肿瘤(癌症)患者之家