MicroRNA-mediated autophagy regulation in thyroid cancer drug resistance.

IF 4.6 Q1 ONCOLOGY

癌症耐药(英文) Pub Date : 2025-06-18 eCollection Date: 2025-01-01 DOI:10.20517/cdr.2025.73

Dongye Huang, Qianwen Liu, Chang Liu, Jingna Cao, Senmin Zhang, Huijiao Cao, Wenkuan Chen

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Abstract

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.

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微rna介导的甲状腺癌耐药自噬调控。

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。尽管治疗策略取得了进步，但耐药性严重阻碍了临床结果。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来矛盾地发挥作用，从而影响治疗耐药性。越来越多的证据表明，通过精确调节自噬相关基因（ATGs）和信号通路，小的非编码rna （microRNAs）是自噬的关键调节因子。miRNA介导的自噬既可以增强化疗疗效，也可以促进耐药，这取决于细胞背景和miRNA靶点。这篇综述总结了最近关于甲状腺癌耐药的mirna -自噬相互作用的见解，强调了关键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克服难治性甲状腺癌耐药的新治疗策略提供了有希望的途径。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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癌症耐药(英文)

CiteScore

6.60

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0.00%

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