AccScience Publishing / TD / Online First / DOI: 10.36922/TD025280062
ORIGINAL RESEARCH ARTICLE

Overcoming cisplatin resistance in ovarian cancer by targeting IFIT1-mediated inflammation responses

Min Hu1 Xuejiao Zhao2 Xiuming Li2 Bin Liu2* Chunluan Yuan3*
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1 Hubei Key Laboratory for Kidney Disease Pathogenesis and Intervention, Hubei Polytechnic University School of Medicine, Huangshi, Hubei, China
2 Jiangsu Key Laboratory of Marine Pharmaceutical Compound Screening, College of Pharmacy, Jiangsu Ocean University, Lianyungang, Jiangsu, China
3 Department of Oncology, The First People’s Hospital of Lianyungang, Lianyungang, Jiangsu, China
Tumor Discovery, 025280062 https://doi.org/10.36922/TD025280062
Received: 8 July 2025 | Revised: 3 September 2025 | Accepted: 26 September 2025 | Published online: 6 November 2025
© 2025 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/ )
Abstract

Ovarian cancer is a highly lethal malignancy, with treatment efficacy frequently compromised by the development of cisplatin resistance. This study investigates the molecular mechanisms driving cisplatin resistance, focusing on interferon-induced protein with tetratricopeptide repeats 1 (IFIT1), a key interferon-stimulated gene. Through comprehensive transcriptome profiling, we systematically compared gene expression patterns between cisplatin-sensitive and cisplatin-resistant ovarian cancer cells, identifying a consistent upregulation of IFIT1 in resistant cells. Functional assays provided evidence that IFIT1 plays a central role in mediating cisplatin resistance. Mechanistically, IFIT1 was found to be associated with activation of inflammatory signaling pathways, suggesting its involvement in resistance-related immune regulation. Clinically, elevated IFIT1 expression significantly correlated with an unfavorable prognosis in ovarian cancer patients. Moreover, we demonstrated that hypoxia-inducible factor-1 alpha transcriptionally regulates IFIT1, linking its expression to hypoxia response. Overall, these findings identify IFIT1 as a key driver of cisplatin resistance in ovarian cancer, shedding light on its clinical significance and the regulatory networks underpinning therapy resistance. IFIT1 holds promise both as a prognostic indicator and as a target for therapeutic intervention. However, its clinical translation will depend on rigorous validation and in-depth exploration.

Keywords
Cisplatin resistance
Ovarian cancer
Interferon-induced protein with tetratricopeptide repeats 1
Gene expression
Inflammatory pathways
Hypoxia
Funding
This study was supported by the Research Foundation of Hubei Polytechnic University (21xjz06A).
Conflict of interest
The authors declare they have no competing interests.
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Tumor Discovery, Electronic ISSN: 2810-9775 Print ISSN: 3060-8597, Published by AccScience Publishing