ZFP36通过破坏非小细胞肺癌中的脂滴积聚来逆转化疗耐药

IF 3.7 2区生物学 Q2 CELL BIOLOGY

Cellular signalling Pub Date : 2025-09-12 DOI:10.1016/j.cellsig.2025.112119

Zhe Wang , Peng Hou , Yang Wu , Jiaojiao Dai , Ping Zhao , Xiaoxun Cheng , Zhengze Hu , Lingling Zhang , Jinghan Hua

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引用次数: 0

摘要

获得性化疗耐药是导致非小细胞肺癌（NSCLC）治疗失败的主要因素，目前尚无有效的干预靶点。最近的证据表明，破坏改变的脂质代谢可能使癌细胞对化疗敏感。本研究表明，锌指蛋白36 （ZFP36）下调通过ZFP36介导的脂肪酸合酶（FASN） mRNA衰变过程促进脂滴（ld）的积累，促进NSCLC的进展和获得化疗耐药。基于ZFP36在化疗耐药中的新调控机制，我们建议通过增强ZFP36对LDs积累的抑制作用来治疗化疗耐药NSCLC。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

ZFP36 reverses chemoresistance by disrupting lipid droplets accumulation in non-small cell lung cancer

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ZFP36 reverses chemoresistance by disrupting lipid droplets accumulation in non-small cell lung cancer

Acquired chemoresistance is a major factor contributing to non-small cell lung cancer (NSCLC) therapy failure, and there is no effective intervention target. Recent evidence suggests that disrupting the altered lipid metabolism could sensitize cancer cells to chemotherapy treatments. Here, we demonstrate that zinc finger protein 36 (ZFP36) downregulation promotes the accumulation of lipid droplets (LDs) through the ZFP36-mediated fatty acid synthase (FASN) mRNA decay process, contributing to NSCLC progression and the acquisition of chemoresistance. We advocate that enhancing the suppressive role of ZFP36 on LDs accumulation to treat chemoresistant NSCLC, based on its novel regulatory mechanism in chemoresistance.

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来源期刊

Cellular signalling 生物-细胞生物学

CiteScore

8.40

自引率

0.00%

发文量

250

审稿时长

27 days

期刊介绍： Cellular Signalling publishes original research describing fundamental and clinical findings on the mechanisms, actions and structural components of cellular signalling systems in vitro and in vivo. Cellular Signalling aims at full length research papers defining signalling systems ranging from microorganisms to cells, tissues and higher organisms.