Huang Dongye, Liu Qianwen, Liu Chang, Cao Jingna, Zhang Senmin, Cao Huijiao, Chen Wenkuan
State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou 510060, Guangdong, China.
Authors contributed equally.
Cancer Drug Resist. 2025 Jun 18;8:30. doi: 10.20517/cdr.2025.73. eCollection 2025.
Thyroid cancer, particularly papillary thyroid cancer (PTC), represents the most prevalent endocrine malignancy. Despite advancements in therapeutic strategies, drug resistance significantly hampers clinical outcomes. Autophagy, an evolutionarily conserved cellular degradation pathway, acts paradoxically in thyroid cancer by promoting either tumor cell survival or cell death, thus influencing therapeutic resistance. Increasing evidence highlights microRNAs (miRNAs), small non-coding RNAs, as critical regulators of autophagy through precise modulation of autophagy-related genes (ATGs) and signaling pathways. miRNA-mediated autophagy can either enhance chemotherapeutic efficacy or facilitate resistance, depending on the cellular context and miRNA targets. This review summarizes recent insights into miRNA-autophagy interactions underlying drug resistance in thyroid cancer, emphasizing key miRNAs, including miR-125b, miR-144, miR-30d, and miR-9-5p. Understanding the complex regulatory networks connecting miRNAs and autophagy provides promising avenues for developing novel therapeutic strategies to overcome resistance in refractory thyroid cancer.
甲状腺癌，尤其是乳头状甲状腺癌（PTC），是最常见的内分泌恶性肿瘤。尽管治疗策略有所进步，但耐药性严重阻碍了临床疗效。自噬是一种进化上保守的细胞降解途径，在甲状腺癌中通过促进肿瘤细胞存活或细胞死亡发挥矛盾作用，从而影响治疗耐药性。越来越多的证据表明，微小RNA（miRNA），即小的非编码RNA，通过精确调节自噬相关基因（ATG）和信号通路，成为自噬的关键调节因子。miRNA介导的自噬根据细胞背景和miRNA靶点，既可以增强化疗疗效，也可以促进耐药性。本综述总结了甲状腺癌耐药性中miRNA-自噬相互作用的最新见解，重点介绍了关键的miRNA，包括miR-125b、miR-144、miR-30d和miR-9-5p。了解连接miRNA和自噬的复杂调控网络为开发新的治疗策略以克服难治性甲状腺癌的耐药性提供了有希望的途径。
