ArticleOncology research2025
3-O-Acetyl-11-Keto-
Article in Oncology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Cytotoxic Activity ofInternational journal of molecular sciences · 2026Article
- Formulation, Characterization, and In Vitro Biological Evaluation of a Triple-Phytochemical Nano Delivery System for Colon Cancer Therapy-A Preliminary Feasibility Study.Pharmaceutics · 2026Article
- HO-1 Up-regulation and PINK1/Parkin-Mediated Mitophagy Contribute to the Anti-tumor Effects of Metochalcone in Colorectal Cancer.Research (Washington, D.C.) · 2026Article
- Molecular structure of 3-Beilstein journal of organic chemistry · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Colorectal cancer (CRC) is one of the most common cancers all over the world. The progression of CRC is associated with inflammation and disruptions in intestinal flora. 3-O-Acetyl-11-keto-β-boswellic acid (AKBA) has been noted for its potent anti-inflammatory properties. However, the effect of AKBA on colon cancer caused by inflammation and its mechanism are not unclear. The study is to explore the effect of AKBA on CRC and its mechanism. Materials and Methods: Cell proliferation, (5-ethynyl-2 Results: Our results showed that AKBA reduced the proliferation of HCT116 and SW620 cells, increased apoptosis of cells, and arrested the cell cycle at the G2/M phase. Results from RNA-seq showed that AKBA inhibited CRC by inhibiting the NF-κB signaling pathway and reducing cellular inflammation. Furthermore, AKBA reduced the levels of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), Interferon-γ (IFN-γ), Interleukin-IL-12p70 (IL-12p70), Interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) in both the spleen and serum of LPS-induced acute inflammation mice. Additionally, AKBA inhibited the development of AOM/DSS-induced colitis-associated colon cancer in mice and positively influenced gut microbiota. Conclusion: This study highlights the inhibitory effect of AKBA on colitis-associated CRC and reveals a novel aspect of its role in the remodeling of gut microbiota. These findings suggest that AKBA may be used as a potential therapeutic agent for CRC.
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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.