ArticleChinese journal of integrative medicine2026
Gancao Ganjiang Decoction Inhibits Renal Cell Carcinoma Progression via PI3K-AKT and JAK-STAT Signaling Pathways.
Article in Chinese journal of integrative medicine, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo evaluate the therapeutic potential of Chinese medicine prescription Gancao Ganjiang Decoction (Licorice and Dried Ginger Decoction, LDGD) against renal cell carcinoma (RCC) and to elucidate its underlying mechanisms.
methodsA mouse RCC model was established in BALB/c mice by subcutaneous injection of Renca cells. The effects of LDGD (5, 10, and 15 g/kg), cisplatin (3 mg/kg), and their combination (10 g/kg LDGD + 3 mg/kg cisplatin) on tumor growth were assessed. Ki-67 expression in tumor tissue was detected by immunohistochemistry. The anti-proliferative effects of LDGD and its 7 blood-absorbed constituents were evaluated on 769-P and 786-O human RCC cell lines using MTT and colony formation assays. Network pharmacology was conducted to predict core targets and signaling pathways. Molecular docking was performed to forecast interactions between active components of LDGD and key proteins in related signaling pathways. Western blot was used to validate phosphorylation levels of the key proteins.
resultsLDGD and cisplatin inhibited mouse RCC growth in vivo. The combination of LDGD with cisplatin enhanced the tumor inhibition rate as compared with cisplatin alone. Ki-67 expression was reduced following treatments. LDGD and its blood-absorbed constituents inhibited RCC cell viability and proliferation in a time- and dose-dependent manner in vitro. Network pharmacology showed that PI3K-AKT and JAK-STAT pathways implicated in the anti-RCC effect of LDGD and its blood-absorbed constituents, and AKT1 and STAT3 were potential targets. Molecular docking suggested that isoliquiritigenin and 6-shogaol had strong binding affinity for AKT1 and STAT3. Western blot showed that LDGD suppressed phosphorylation of AKT and STAT3 in 769-P cells, while inhibited phosphorylation of STAT3 protein in 786-O cells. Isoliquiritigenin inhibited phosphorylation of AKT and STAT3 proteins in both 769-P and 786-O cells, and 6-shogaol inhibited phosphorylation of STAT3 protein in 786-O cells.
conclusionLDGD exerts significant anti-tumor effects against RCC, possibly via suppression of AKT and STAT3 phosphorylation.
Indexed as
Identifiers
42455419What Socratic 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 Socratic graph.