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Epigenetic-based combination therapy and liposomal codelivery overcomes osimertinib-resistant NSCLC via repolarizing tumor-associated macrophages

Ting-ting Lin1,2, Wei Xiong3,4, Gui-hua Chen2,3, Yang He2, Li Long2, Xin-fu Gao1, Jia-lin Zhou4, Wen-wen Lv1, Yong-zhuo Huang2,3,4,5
1 Department of Pharmacy, Binzhou Medical University Hospital, Binzhou 256603, China
2 State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China
3 Artemisinin Research Center, Guangzhou University of Chinese Medicine, Guangzhou 510450, China
4 Zhongshan Institute for Drug Discovery, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Zhongshan 528437, China
5 NMPA Key Laboratory for Quality Research and Evaluation of Pharmaceutical Excipients, Shanghai 201203, China
Correspondence to: Wen-wen Lv: byyxlww@126.com, Yong-zhuo Huang: yzhuang@simm.ac.cn,
DOI: 10.1038/s41401-023-01205-4
Received: 22 July 2023
Accepted: 19 November 2023
Advance online: 19 December 2023

Abstract

Osimertinib (Osi) is widely used as a first-line treatment for non-small cell lung cancer (NSCLC) with EGFR mutations. However, the majority of patients treated with Osi eventually relapse within a year. The mechanisms of Osi resistance remain largely unexplored, and efficient strategies to reverse the resistance are urgently needed. Here, we developed a lactoferrin-modified liposomal codelivery system for the combination therapy of Osi and panobinostat (Pan), an epigenetic regulator of histone acetylation. We demonstrated that the codelivery liposomes could efficiently repolarize tumor-associated macrophages (TAM) from the M2 to M1 phenotype and reverse the epithelial-mesenchymal transition (EMT)-associated drug resistance in the tumor cells, as well as suppress glycolysis, lactic acid production, and angiogenesis. Our results suggested that the combination therapy of Osi and Pan mediated by liposomal codelivery is a promising strategy for overcoming Osi resistance in NSCLC.
Keywords: osimertinib resistance; targeted drug delivery; liposomes; panobinostat; tumor-associated macrophage; combination therapy

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