ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
B-AP15 inhibited colon cancer cell proliferation by decreasing CDK6, Cyclin A, Cyclin E, c-Myc, and VEGF gene expression.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed.
- Artificial Gap Junctional Channel Inhibiting the Proliferation of Hepatocellular Carcinoma Cells.Angewandte Chemie (International ed. in English) · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
This study evaluated the screening of novel possible target proteins of B-AP15 (NSC687852) in silico. Through in vitro investigation, the anticancer activity of B-AP15 was examined with respect to gene expression and cell proliferation of SW620 cells (colon cancer cells). Twenty proteins associated with colon cancer were selected to screen possible target proteins of B-AP15 using molecular docking. The binding position of B-AP15 and the top five candidate proteins were investigated using the Discovery Studio 2021 software program. Cytotoxicity, colonization ability, and cell inhibition were evaluated in SW620 cells for 24, 48, and 72 h via MTT assay, colony formation assay, and trypan blue assay. The gene expression was estimated using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) at 48 h. B-AP15 showed higher binding to E2F8 (- 10.88 kcal/mol), Ras (- 10.86 kcal/mol), GSK3B (- 10.77 kcal/mol), CDK6 (- 10.75 kcal/mol), and Raf (- 10.12 kcal/mol) than to USP14 (- 7.83 kcal/mol) as a target protein of B-AP15. Interestingly, Ras, GSK3B, and CDK6 shared the binding position between B-AP15 and known inhibitors. The IC
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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 OpenQuestion graph.