Cholesterol confers resistance to Apatinib-mediated ferroptosis in gastric cancer

Abstract Background Gastric cancer is the fifth leading cause of cancer-related deaths worldwide. Apatinib is a third-line treatment for gastric cancer. However, the development of resistance significantly limits its efficacy, and effective and safe strategies to overcome Apatinib resistance remain...

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Main Authors: Zhiwei Li, Chenxin Liu, Minghao Wang, Riqing Wei, Ru Li, Kaihua Huang, Huayuan Liang, Guoxin Li, Liying Zhao
Format: Article
Language:English
Published: BMC 2025-07-01
Series:Cell & Bioscience
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Online Access:https://doi.org/10.1186/s13578-025-01435-5
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author Zhiwei Li
Chenxin Liu
Minghao Wang
Riqing Wei
Ru Li
Kaihua Huang
Huayuan Liang
Guoxin Li
Liying Zhao
author_facet Zhiwei Li
Chenxin Liu
Minghao Wang
Riqing Wei
Ru Li
Kaihua Huang
Huayuan Liang
Guoxin Li
Liying Zhao
author_sort Zhiwei Li
collection DOAJ
description Abstract Background Gastric cancer is the fifth leading cause of cancer-related deaths worldwide. Apatinib is a third-line treatment for gastric cancer. However, the development of resistance significantly limits its efficacy, and effective and safe strategies to overcome Apatinib resistance remain elusive. Results We found that Apatinib-resistant gastric cancer cells (MGC803/AR and AGS/AR) exhibited increased cholesterol synthesis and elevated intracellular cholesterol levels, which contributed to Apatinib resistance. Further investigation identified 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) as one of the most upregulated genes in the cholesterol synthesis pathway. Inhibition of HMGCR not only suppressed the proliferation, migration, and invasion of resistant cells but also reduced their resistance to Apatinib. Moreover, Simvastatin, an HMGCR inhibitor, effectively resensitized resistant cells to Apatinib-induced ferroptosis, thereby enhancing the therapeutic efficacy of Apatinib both in vitro and in vivo. Conclusions These findings suggest that Simvastatin may serve as a novel and safe strategy to overcome Apatinib resistance in gastric cancer.
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issn 2045-3701
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publishDate 2025-07-01
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spelling doaj-art-602a6f12201a4bba9799e3db33159d5b2025-08-20T03:42:00ZengBMCCell & Bioscience2045-37012025-07-0115111910.1186/s13578-025-01435-5Cholesterol confers resistance to Apatinib-mediated ferroptosis in gastric cancerZhiwei Li0Chenxin Liu1Minghao Wang2Riqing Wei3Ru Li4Kaihua Huang5Huayuan Liang6Guoxin Li7Liying Zhao8Department of General Surgery, Nanfang Hospital, The First School of Clinical Medicine, Southern Medical UniversityDepartment of Clinical Laboratory, National Center for Respiratory Medicine, National Clinical Research Center for Respiratory Disease, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical UniversityDepartment of General Surgery, Nanfang Hospital, The First School of Clinical Medicine, Southern Medical UniversityDepartment of Biopharmaceutics, School of Laboratory Medicine and Biotechnology, Southern Medical UniversityDepartment of Biopharmaceutics, School of Laboratory Medicine and Biotechnology, Southern Medical UniversityDepartment of General Surgery, Nanfang Hospital, The First School of Clinical Medicine, Southern Medical UniversityDepartment of Gastrointestinal Surgery, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua UniversityDepartment of General Surgery, Nanfang Hospital, The First School of Clinical Medicine, Southern Medical UniversityDepartment of General Surgery, Nanfang Hospital, The First School of Clinical Medicine, Southern Medical UniversityAbstract Background Gastric cancer is the fifth leading cause of cancer-related deaths worldwide. Apatinib is a third-line treatment for gastric cancer. However, the development of resistance significantly limits its efficacy, and effective and safe strategies to overcome Apatinib resistance remain elusive. Results We found that Apatinib-resistant gastric cancer cells (MGC803/AR and AGS/AR) exhibited increased cholesterol synthesis and elevated intracellular cholesterol levels, which contributed to Apatinib resistance. Further investigation identified 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) as one of the most upregulated genes in the cholesterol synthesis pathway. Inhibition of HMGCR not only suppressed the proliferation, migration, and invasion of resistant cells but also reduced their resistance to Apatinib. Moreover, Simvastatin, an HMGCR inhibitor, effectively resensitized resistant cells to Apatinib-induced ferroptosis, thereby enhancing the therapeutic efficacy of Apatinib both in vitro and in vivo. Conclusions These findings suggest that Simvastatin may serve as a novel and safe strategy to overcome Apatinib resistance in gastric cancer.https://doi.org/10.1186/s13578-025-01435-5Gastric cancerApatinibFerroptosisCholesterolHMGCR
spellingShingle Zhiwei Li
Chenxin Liu
Minghao Wang
Riqing Wei
Ru Li
Kaihua Huang
Huayuan Liang
Guoxin Li
Liying Zhao
Cholesterol confers resistance to Apatinib-mediated ferroptosis in gastric cancer
Cell & Bioscience
Gastric cancer
Apatinib
Ferroptosis
Cholesterol
HMGCR
title Cholesterol confers resistance to Apatinib-mediated ferroptosis in gastric cancer
title_full Cholesterol confers resistance to Apatinib-mediated ferroptosis in gastric cancer
title_fullStr Cholesterol confers resistance to Apatinib-mediated ferroptosis in gastric cancer
title_full_unstemmed Cholesterol confers resistance to Apatinib-mediated ferroptosis in gastric cancer
title_short Cholesterol confers resistance to Apatinib-mediated ferroptosis in gastric cancer
title_sort cholesterol confers resistance to apatinib mediated ferroptosis in gastric cancer
topic Gastric cancer
Apatinib
Ferroptosis
Cholesterol
HMGCR
url https://doi.org/10.1186/s13578-025-01435-5
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AT riqingwei cholesterolconfersresistancetoapatinibmediatedferroptosisingastriccancer
AT ruli cholesterolconfersresistancetoapatinibmediatedferroptosisingastriccancer
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