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Apolipoprotein B100 acts as a tumor suppressor in ovarian cancer via lipid/ER stress axis-induced blockade of autophagy

Acta Pharmacologica Sinica volume 46, pages 1445–1461 (2025)Cite this article

Abstract

Ovarian cancer presents a significant treatment challenge due to its insidious nature and high malignancy. As autophagy is a vital cellular process for maintaining homeostasis, targeting the autophagic pathway has emerged as an avenue for cancer therapy. In the present study, we identify apolipoprotein B100 (ApoB100), a key modulator of lipid metabolism, as a potential prognostic biomarker of ovarian cancer. ApoB100 functioned as a tumor suppressor in ovarian cancer, and the knockdown of ApoB100 promoted ovarian cancer progression in vivo. Moreover, ApoB100 blocked autophagic flux, which was dependent on interfering with the lipid accumulation/endoplasmic reticulum (ER) stress axis. The effects of LFG-500, a novel synthetic flavonoid, on ApoB100 induction were confirmed using proteomics and lipidomics analyses. Herein, LFG-500 induced lipid accumulation and ER stress and subsequently blocked autophagy by upregulating ApoB100. Moreover, data from in vivo experiments further demonstrated that ApoB100, as well as the induction of the lipid/ER stress axis and subsequent blockade of autophagy, were responsible for the anti-tumor effects of LFG-500 on ovarian cancer. Hence, our findings support that ApoB100 is a feasible target of ovarian cancer associated with lipid-regulated autophagy and provide evidence for using LFG-500 for ovarian cancer treatment.

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Fig. 1: ApoB100 is a potential prognostic biomarker of ovarian cancer.
Fig. 2: Identification of ApoB100 as a tumor suppressor in ovarian cancer.
Fig. 3: ApoB100 knockdown promotes the proliferation of ovarian cancer cells.
Fig. 4: ApoB100 suppresses ovarian cancer by blocking autophagy through the induction of the lipid/ER stress axis.
Fig. 5: Proteomics and lipidomics analyses identify LFG-500 as an ApoB100 inducer.
Fig. 6: LFG-500 suppresses ovarian cancer cells in vitro and in vivo.
Fig. 7: LFG-500 suppresses ovarian cancer through blockade of autophagy.
Fig. 8: LFG-500 upregulates ApoB100 expression to promote lipid/ER stress axis.
Fig. 9: Targeting ApoB100 by LFG-500 against ovarian cancer.
Fig. 10: Schematic diagram of LFG-500 inhibiting autophagy.

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Acknowledgements

We thank Prof. Qing-long Guo from China Pharmaceutical University for the generous provision of LFG-500. We also thank Dr. Xue Zhao for her dedicated contributions as an advisor/expert for the whole story with invaluable insights and innovative ideas. We also extend our gratitude to Prof. Wu-yang Wang and Dr. Yan-hong Xing for their insightful guidance and expertise in the field of autophagy. We sincerely thank Dr. Fu-xing Dong from the Public Experimental Research Center for his enthusiastic help in the experiment of laser scanning confocal microscopy. Additionally, we are thankful for the contributions of Ms. Gui-xiang Xiong for her support as a technician/expert. We would like to thank MogoEdit (https://www.mogoedit.com) for its English editing during the preparation of this manuscript.

Funding

This study was supported by the Jiangsu Province Traditional Chinese Medicine Science Foundation (ZT202114), the Jiangsu Province Science and Technology Project (BE2019636), the Guangdong Basic and Applied Basic Research Foundation (2024A1515013108), the Medical Joint Fund of Jinan University (YXJC2022002), the Fundamental Research Funds for the Central Universities (21623109), and the Xuzhou Clinical Expert Team Introduction Project (2019TD005).

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  1. These authors contributed equally: Ze-yuan Yin, Shi-min He

Authors and Affiliations

  1. The First Clinical Medical School, Xuzhou Medical University, Xuzhou, 221004, China

    Ze-yuan Yin & Bing-xuan Hu

  2. Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou Medical University, Xuzhou, 221004, China

    Ze-yuan Yin, Xin-yuan Zhang, Xiao-chen Yu, Kai-xuan Sheng, Liu Xu, Bei-bei Zhang, Xue-yan Zhou, Bei Zhang & Cheng-lin Li

  3. Department of Cardiology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221004, China

    Ze-yuan Yin

  4. Cardiovascular Sciences, The University of Manchester, Manchester, M13 9NT, UK

    Ze-yuan Yin

  5. Department of Obstetrics and Gynecology, Xuzhou Central Hospital, Xuzhou Clinical School of Xuzhou Medical University, Xuzhou, 221009, China

    Shi-min He, Tong Fu, Jing-bo Zhang, Yan-yu Li, Qing Wang, Yun-meng Qi & Bei Zhang

  6. Department of Obstetrics and Gynecology, Zhenjiang Fourth People’s Hospital, Zhenjiang, 212001, China

    Shi-min He

  7. Xuzhou Center for Disease Control and Prevention, Xuzhou, 221002, China

    Yi-xue Jiang

  8. Department of Physiology, Xuzhou Medical University, Xuzhou, 221004, China

    Joseph Adu-Amankwaah

  9. State Key Laboratory of Bioactive Molecules and Drug Ability Assessment; MOE Key Laboratory of Tumor Molecular Biology; Guangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research; Department of Pharmacology, School of Medicine, Jinan University, Guangzhou, 510632, China

    Qi Qi

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Contributions

CLL, BZ, QQ, and ZYY conceived the project, designed the experiments, and revised the manuscript. ZYY and SMH performed major experiments, analyzed major data and wrote the manuscript. XYZ (Xin-yuan Zhang), XCY and KXS performed a part of Western blot. TF and BXH performed a part of immunohistochemistry. XYZ (Xin-yuan Zhang), LX and YXJ performed the bioinformatics analysis. JAA, YMQ, JBZ, YYL, QW, BBZ and XYZ (Xue-yan Zhou) helped with the analysis.

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Correspondence to Qi Qi, Bei Zhang or Cheng-lin Li.

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Yin, Zy., He, Sm., Zhang, Xy. et al. Apolipoprotein B100 acts as a tumor suppressor in ovarian cancer via lipid/ER stress axis-induced blockade of autophagy. Acta Pharmacol Sin 46, 1445–1461 (2025). https://doi.org/10.1038/s41401-024-01470-x

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