Evidence map›Paper›PMID 41784696›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2026

Citronellol potentiates sunitinib efficacy in renal cell carcinoma by targeting JAK2/STAT3 signaling pathway.

Zongrun Sun, Zixuan Chen, Yuesong Cai, Guohuan Yin, Ya Song, Xing Jia, Min Liu

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Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Zongrun Sun *Department of Urology, Tongren Hospital Shanghai Jiao Tong University School of Medicine, No.1111 Xian Xia Road, Shanghai, 200336, China.
Zixuan Chen *Department of Urology, Tongren Hospital Shanghai Jiao Tong University School of Medicine, No.1111 Xian Xia Road, Shanghai, 200336, China.
Yuesong Cai *College of Medicine, Yanbian University, Yanji, 133002, China.
Guohuan YinCenter for Rare Diseases, State Key Laboratory of Complex, Severe, and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, 100730, China.
Ya SongSchool of Life Sciences, Bengbu Medical University, Bengbu, 233000, China.
Xing JiaDepartment of Urology, Tongren Hospital Shanghai Jiao Tong University School of Medicine, No.1111 Xian Xia Road, Shanghai, 200336, China. jiaxing92222@163.com.
Min LiuDepartment of Urology, Tongren Hospital Shanghai Jiao Tong University School of Medicine, No.1111 Xian Xia Road, Shanghai, 200336, China. lm4104@shtrhospital.com.

Funding

National Natural Science Foundation of China No. 82172809
6 · The paper itself

Abstract

Renal cell carcinoma. (RCC) is the most common form of kidney cancer and frequently develops resistance to tyrosine kinase inhibitors (TKIs), such as sunitinib, limiting treatment efficacy. To address this challenge, we investigated the potential of Citronellol, a plant-derived monoterpenoid, to enhance sunitinib sensitivity in RCC. Through network pharmacology analysis, the potential targets of Citronellol were identified, and it was confirmed that it may exert anticancer effects through the EGFR and JAK2/STAT3 signaling pathways. In vitro experimental results showed that Citronellol significantly inhibited the proliferation and migration of 786-O and A498 cells and induced apoptosis. Furthermore, when combined with sunitinib treatment, Citronellol significantly reduced the IC50 value of sunitinib and enhanced its inhibitory effect on renal cancer cells. Western blot results further revealed that Citronellol significantly inhibited the phosphorylation of EGFR, JAK2, and STAT3, suggesting that it may enhance the anticancer activity of sunitinib by inhibiting the survival signals mediated by the JAK2/STAT3 signaling pathway. This study is the first to systematically reveal that Citronellol enhances the therapeutic effect of sunitinib in RCC cells by modulating the JAK2/STAT3 signaling pathways. These findings suggest a promising combination strategy for overcoming TKI resistance and improving RCC treatment outcomes.

Indexed as

Acyclic MonoterpenesAntineoplastic AgentsCarcinoma, Renal CellJanus Kinase 2Kidney NeoplasmsSTAT3 Transcription FactorSunitinibAntineoplastic Combined Chemotherapy ProtocolsApoptosisCell Line, TumorCell MovementCell ProliferationDrug SynergismErbB ReceptorsHumansSignal TransductionAcyclic MonoterpenesAntineoplastic AgentscitronellolErbB ReceptorsJAK2 protein, humanJanus Kinase 2STAT3 protein, humanSTAT3 Transcription FactorSunitinibTyrosine Kinase InhibitorsCitronellolJAK2/STAT3 signaling pathwaysNetwork pharmacologyRenal Cell CarcinomaSunitinib

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.