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ARTICLE

Synergistic Antitumour Effects of Harringtonine and Cresatin against Non-Small Cell Lung Cancer In Vitro and In Vivo

Chi-Hsuan Wei1, Pei-Yu Lin1, Chia-Wei Weng1,2, Meng-Fang Tsai3, Jeremy J. W. Chen1,4,*
1 Graduate Institute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan
2 Department of Surgery, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei City, Taiwan
3 Department of Biomedical Sciences, Da-Yeh University, Changhua, Taiwan
4 Graduate Institute of Molecular Biology, National Chung Hsing University, Taichung, Taiwan
* Corresponding Author: Jeremy J. W. Chen. Email: email
(This article belongs to the Special Issue: Pharmacological Bases of Anticancer Drug Therapies in Precision Oncology)

Oncology Research https://doi.org/10.32604/or.2026.081088

Received 23 February 2026; Accepted 17 August 2026; Published online 20 August 2026

Abstract

Objectives: Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related deaths, largely due to late diagnosis, frequent metastasis, and acquired resistance to tyrosine kinase inhibitors (TKIs). Upregulation of epidermal growth factor receptor (EGFR) and Src promotes tumour progression, highlighting them as potential therapeutic targets. This study aims to investigate novel strategies to overcome tyrosine kinase inhibitor (TKI) resistance and improve NSCLC treatment outcomes. Methods: In this study, harringtonine and cresatin were identified using a previously established pharmacophore model and an enzyme-linked immunosorbent assay (ELISA)-based screening approach, respectively. NSCLC cell lines harbouring different EGFR genotypes were used to evaluate the inhibitory effects of harringtonine and cresatin on cell proliferation, migration, and invasion. Furthermore, in vitro assays and xenograft animal models were employed to validate the therapeutic potential of the combination treatment. Results: In vitro experiments demonstrated that both harringtonine and cresatin significantly reduced cell viability, proliferation, invasion, migration, and colony formation across NSCLC cell lines harbouring various EGFR genotypes. Treatment with harringtonine or cresatin also decreased the expression of EGFR- and Src-related signalling proteins. Notably, harringtonine and cresatin altered the phenotype of drug-resistant H1975 cells by reducing the activity of Rho GTPase proteins. Moreover, the combination of harringtonine and cresatin not only resulted in a lower dose but also synergistically inhibited tumour growth in vivo by suppressing the activity of the EGFR- and Src-associated pathways. Conclusion: Our findings highlight the use of harringtonine and cresatin as promising agents for the clinical treatment of NSCLC and offer new insights into drug repurposing strategies.

Keywords

NSCLC; EGFR; Src; targeted therapy; combination therapy; harringtonine; cresatin

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