A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Artesunate Nanoplatform Targets the Serine–MAPK Axis in Cancer‐Associated Fibroblasts to Reverse Photothermal Resistance in Triple‐Negative Breast Cancer
Tekijät: Zheng, Dongdong; Yan, Jiaqi; Liu, Xuejiao; Zhang, Zhiming; Jin, Anqi; Zhao, Yue; Bai, Lu; Quan, Mengyao; Qi, Xiuzhu; Fu, Bin; Wu, Zhigang; Zhou, Jin; Han, Han; Wang, Ziqi; Wang, Shiyu; Deng, Chaoqiang; Sun, Weijian; Chang, Cai; Zhou, Shichong; Zhang, Hongbo
Kustantaja: Wiley
Kustannuspaikka: WEINHEIM
Julkaisuvuosi: 2025
Journal: Advanced Materials
Tietokannassa oleva lehden nimi: Advanced Materials
Lehden akronyymi: ADV MATER
Artikkelin numero: 2502617
Vuosikerta: 37
Sivujen määrä: 22
ISSN: 0935-9648
eISSN: 1521-4095
DOI: https://doi.org/10.1002/adma.202502617
Verkko-osoite: https://doi.org/10.1002/adma.202502617
Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/detail/Publication/499520637
Cancer-associated fibroblasts (CAFs) play a pivotal role in inducing photothermal therapy (PTT) resistance of triple-negative breast cancer (TNBC), but with unclear mechanism. Herein, aminoethyl anisamide-modified nano-biomimetic low-density lipoprotein (A-aLDL) is used to target deliver the PTT agent and artesunate (ARS) to both CAFs and cancer cells. Though CAFs are sensitive to PTT and notably transition to heat-resistant phenotype, the formed protective barrier is destroyed by ARS. Subsequently, the outstanding anti-tumor effects are achieved through PTT in multiple models with such kind of combination therapy. Interestingly, the mechanism is discovered that serine metabolism plays a major role in CAF resistance through spatially omics. ARS disrupts serine homeostasis, thereby attenuating the cascade activity of GTPases in MAPK pathway. Meanwhile, MAP2K7 is the most potential target for sensitizing PTT. By integrating ARS with PTT agents, the serine-MAPK axis in CAFs is successfully modulated, thereby overcoming PTT resistance in TNBC therapy.
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This study was supported by the National Science Foundation (Grant No. 82372145 (H.Z.)), the Joint Fund of the Zhejiang Provincial Natural Science Foundation of China (Grant No. BD24H180004 (H.Z.)), and the grant from the Discipline Cluster of Oncology, Wenzhou Medical University, China (Grant No. z1-2023002 (H.Z.)). It was also supported by the Research Project (Grant No. 347897 (H.Z.)), Solution for Health Profile (Grant No. 336355 (H.Z.)), InFLAMES Flagship (Grant No. 337531 (H.Z.)) and Printed Intelligence Infrastructure (PII-FIRI) from Research Council of Finland. The National Natural Science Foundation of China (Grant No. 82071945, 82371978, 82311530049 (S.Z.)), Shanghai Committee of Science and Technology, China (Grant No. 21S31905400 (S.Z.)), the National Natural Science Foundation of China (Grant No. 81830058 (C.C.)), and the Shanghai Anticancer Association EYAS PROJECT (Grant No. SACA-CY22C07 (D.Z.)), China Postdoctoral Science Foundation (Grant No. 2024M760561 (D.Z.))
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