ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Citronellol potentiates sunitinib efficacy in renal cell carcinoma by targeting JAK2/STAT3 signaling pathway.
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.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
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
Identifiers
41784696What OpenQuestion holds
Registered trials
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.