ArticleOncology letters2024
Fisetin enhances cisplatin sensitivity in renal cell carcinoma via the CDK6/PI3K/Akt/mTOR signaling pathway.
Article in Oncology letters, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Natural products as kinase inhibitors in lung cancer: molecular mechanisms, therapeutic potential, and clinical trials.Frontiers in pharmacology · 2026Review
- Natural Compounds in Cancer Therapy: Revealing the Role of Flavonoids in Renal Cell Carcinoma Treatment.Biomolecules · 2025Review
- Gallic acid potentiates the anticancer efficacy of cisplatin in ovarian cancer cells through modulation of the PI3K/AKT/mTOR and CXCL12/CXCR4 signaling pathways.Frontiers in oncology · 2025Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin resistance is ubiquitous among patients with renal cell carcinoma (RCC). The present study assessed the role of fisetin in regulating cisplatin sensitivity and increasing the efficacy of chemotherapy for patients with RCC. Cell Counting Kit-8 and colony formation assays were used to assess the proliferation of RCC cells after fisetin and cisplatin treatment. The mRNA expression levels of cyclin-dependent kinase (CDK)6 were evaluated using reverse transcription-quantitative PCR. The expression levels of CDK6 and key proteins of the PI3K/Akt/mTOR signaling pathway were assessed using western blotting. The present study demonstrated that fisetin inhibited the proliferation and colony-forming ability of RCC cells, and induced apoptosis and cell cycle arrest in a dose-dependent manner. Additionally, fisetin enhanced the antineoplastic effects of cisplatin, as demonstrated by the increase in proliferation inhibition and apoptosis promotion after fisetin and cisplatin combination treatment. Furthermore, fisetin regulated the PI3K/Akt/mTOR signaling pathway through CDK6 inhibition, which enhanced cisplatin sensitivity. Overexpression of CDK6 neutralized the positive effects of fisetin on the improvement of cisplatin sensitivity in RCC cells. In conclusion, fisetin may enhance the sensitivity of RCC cells to cisplatin via the CDK6/PI3K/Akt/mTOR signaling pathway.
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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 Socratic graph.