We sincerely thank Shameer Tahir for the interest in
our research and for the thoughtful comments. In this
study, by integrating multi-omics data (transcriptomics,
metabolomics, single-cell) across two cellular models, we
uncovered a novel mechanism of crizotinib resistance in
ROS1+
or ALK+
non-small cell lung cancer (NSCLC),
in which arachidonic acid (AA) promotes autophagy flux
to reduce drug-induced autophagosome accumulation.
Targeting this AA-mediated autophagy with chloroquine
(CQ) effectively restored crizotinib sensitivity, suggesting a
potential therapeutic strategy for overcoming resistance.
语种：
外文
PubmedID：
中科院(CAS)分区：
出版当年[2025]版：
大类|3 区医学
小类|3 区肿瘤学3 区呼吸系统
最新[2025]版：
大类|3 区医学
小类|3 区肿瘤学3 区呼吸系统
第一作者：
第一作者机构：[1]Department of Thoracic Surgery and Institute of Thoracic Oncology, West China Hospital, Sichuan University, Chengdu, China.
通讯作者：
推荐引用方式(GB/T 7714)：
Jie Hui,Lai Hongjin,Wang Zihuai,et al.Arachidonic acid-mediated autophagy regulation drives crizotinib resistance in lung cancer: therapeutic opportunities and challenges[J].Translational Lung Cancer Research.2025,14(7):2893-2894.doi:10.21037/tlcr-2025-615.
APA：
Jie Hui,Lai Hongjin,Wang Zihuai,Liu Lunxu,Deng Senyi&Guo Chenglin.(2025).Arachidonic acid-mediated autophagy regulation drives crizotinib resistance in lung cancer: therapeutic opportunities and challenges.Translational Lung Cancer Research,14,(7)
MLA：
Jie Hui,et al."Arachidonic acid-mediated autophagy regulation drives crizotinib resistance in lung cancer: therapeutic opportunities and challenges".Translational Lung Cancer Research 14..7(2025):2893-2894
