ArticleScientific reports2025
The mechanism of Shancigu and its monomer in the development of colorectal cancer based on network pharmacology.
Article in Scientific reports, 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
8 authors.
Funding
Abstract
Shancigu has traditionally been used for clearing heat, detoxification, resolving phlegm, and dissipating masses. However, its potential mechanisms in colorectal cancer (CRC) remain unclear. This study aimed to explore the molecular mechanisms of Shancigu and its active compound in CRC. The active ingredients of Shancigu and their predicted targets were identified, and differentially expressed genes (DEGs) associated with CRC metastasis and invasion were screened. Intersection genes were obtained and used to construct a protein-protein interaction (PPI) network. Core genes were identified, and their prognostic significance was analyzed. Molecular docking was performed between key survival-related genes and Shancigu compounds. Further in vitro, organoid, and in vivo experiments were conducted to investigate the regulatory effects of Stigmasterol, a major active component. A total of 18 active ingredients and 366 potential targets of Shancigu were identified. From 19,331 DEGs, 365 intersection genes and 18 core genes were screened. Among them, AKT1, AR, FN1, HRAS, ITGB1, and JUN showed significant prognostic relevance in CRC. Molecular docking revealed that Stigmasterol strongly binds to ITGB1 and JUN. In cellular experiments, Stigmasterol inhibited viability, proliferation, migration, and invasion, induced apoptosis, and downregulated JUN and ITGB1 expressions in HCT116 and Caco-2 cells. In CRC organoids, Stigmasterol reduced organoid viability and ATP activity. Animal studies demonstrated that both Shancigu and Stigmasterol reduced tumor weight and volume and inhibited Ki67, ITGB1, and JUN expression. Stigmasterol may suppress CRC proliferation and invasion by targeting the key genes JUN and ITGB1, providing insights into the potential therapeutic mechanisms of Shancigu against CRC.
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.