ArticleMedicine2025
Effective components of Coptidis Rhizoma and Cinnamomi Cortex in the treatment of renal cell carcinoma and their mechanism of action.
Article in Medicine, 2025. 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
5 authors.
Funding
Abstract
This study aimed to investigate the mechanism of the Coptidis Rhizoma and Cinnamomi Cortex (HL-RG) drug pair in the intervention of renal cell carcinoma (RCC) using network pharmacology, molecular docking, and cell experiments. Network pharmacology analysis predicted 42 active components in HL-RG and identified 227 potential targets. Among these, 50 targets were specifically associated with RCC, and 18 were identified as hub genes. Three components (quercetin, oleic acid, tetrandrine) were highlighted as particularly effective. The results of the gene ontology (GO) annotation showed that HL-RG may treat RCC by regulating biological processes such as inflammation, immune response, cell cycle process, and lipid metabolism. Kyoto Gene and Genome Encyclopedia (KEGG) enrichment revealed that the key targets of HL-RG in treating RCC were enriched in the proteoglycans in cancer, and the HIF-1 signaling pathway. Molecular docking results demonstrated that 87% of the interactions exhibited binding energies stronger than -5.0 kcal/mol, indicating favorable binding affinity between the core active components and key targets. Experimental validation using quantitative real-time polymerase chain reaction and Western blot in 786-O cells demonstrated that tetrandrine (TET) and quercetin (QUE) downregulated the mRNA and protein levels of G1/S-specific cyclin-D1 (CCND1) and Transforming growth factor beta-1 (TGFB1), and upregulated the mRNA levels of Catalase (CAT). Additionally, QUE downregulated the mRNA levels of Receptor tyrosine-protein kinase erbB-2 (ERBB2) and upregulated the mRNA levels of Pro-epidermal growth factor (EGF). Furthermore, oleic acid (OA), TET, and QUE downregulated the protein levels of Matrix metalloproteinase-9 (MMP9). In conclusion, the therapeutic effect of the HL-RG combination against RCC is primarily mediated by its bioactive components, QUE, OA, and TET. These components regulate the HIF-1 signaling pathway, activating genes involved in the cellular response to hypoxia and modulating the expression of proteins that control glucose metabolism, cell proliferation, and angiogenesis.
Indexed as
Identifiers
What 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.