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

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Cellular signalling 📖 저널 OA 7.8% 2023: 0/1 OA 2024: 1/14 OA 2025: 2/79 OA 2026: 11/85 OA 2023~2026 2025 Vol.136() p. 112119
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Wang Z, Hou P, Wu Y, Dai J, Zhao P, Cheng X

📝 환자 설명용 한 줄

Acquired chemoresistance is a major factor contributing to non-small cell lung cancer (NSCLC) therapy failure, and there is no effective intervention target.

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APA Wang Z, Hou P, et al. (2025). ZFP36 reverses chemoresistance by disrupting lipid droplets accumulation in non-small cell lung cancer.. Cellular signalling, 136, 112119. https://doi.org/10.1016/j.cellsig.2025.112119
MLA Wang Z, et al.. "ZFP36 reverses chemoresistance by disrupting lipid droplets accumulation in non-small cell lung cancer.." Cellular signalling, vol. 136, 2025, pp. 112119.
PMID 40946947 ↗

Abstract

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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🏷️ 같은 키워드 · 무료전문 — 이 논문 MeSH/keyword 기반