ArticleInternational journal of molecular medicine2020
Asiaticoside suppresses cell proliferation by inhibiting the NF‑κB signaling pathway in colorectal cancer.
Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
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- LAR1 promotes breast carcinogenesis by activating NF-κB signaling pathway through binding and enhancing APOC1 expression.iScience · 2026Article
- Mechanisms and advantages of natural derived small molecule compounds in the prevention and treatment of colorectal cancer: a review.Frontiers in pharmacology · 2025Review
- Asiaticoside inhibits breast cancer progression and tumor angiogenesis via YAP1/VEGFA signal pathway.Heliyon · 2024Article
- UBXN11 Predicts as a Poor Index for Colorectal Cancer and Contributes to the Tumorigenesis by Activating NF-κB Signaling.Digestive diseases and sciences · 2024Article
- Article
- Apiaceae Medicinal Plants in China: A Review of Traditional Uses, Phytochemistry, Bolting and Flowering (BF), and BF Control Methods.Molecules (Basel, Switzerland) · 2023Review
- Asiaticoside Increases Caspase-9 Activity in MCF-7 Cells and Inhibits TNF-α and IL-6 Expression in Nude Mouse Xenografts via the NF-κB Pathway.Molecules (Basel, Switzerland) · 2023Article
- Asiaticoside reverses M2 phenotype macrophage polarization-evoked osteosarcoma cell malignant behaviour by TRAF6/NF-κB inhibition.Pharmaceutical biology · 2022Article
- Origin, evolution, breeding, and omics of Apiaceae: a family of vegetables and medicinal plants.Horticulture research · 2022Article
- Asiaticoside Suppresses Gastric Cancer Progression and Induces Endoplasmic Reticulum Stress through the miR-635/HMGA1 Axis.Journal of immunology research · 2022Article
- Inhibition of hypertrophic scar formation with oral asiaticoside treatment in a rabbit ear scar model.International wound journal · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is one of the leading causes of cancer‑associated mortality. Asiaticoside (AC) exhibits antitumor effects; however, to the best of our knowledge, the biological function of AC in CRC cells remains unclear. Therefore, the aim of the present study was to investigate the effect of AC on CRC cells. In the present study, CCK‑8 and colony formation assays were performed to assess the effects of AV on human CRC cell lines (HCT116, SW480 and LoVo). Mitochondrial membrane potential was examined by JC‑1 staining. Cell apoptosis and cell cycle were monitored by flow cytometry, and the expression of genes was evaluated using RT‑qPCR and western blot analysis. Furthermore, the biological effect of AC in vivo was detected using a xenograft mouse model. The findings revealed that 2 µM AC suppressed the proliferation of CRC cells in a time‑ and dose‑dependent manner, but had no adverse effects on normal human intestinal FHC cells at a range of concentrations. AC decreased the mitochondrial membrane potential and increased the apoptosis of CRC cells in a dose‑dependent manner. Furthermore, AC induced cell cycle arrest at the G0/G1 phase. AC attenuated IκBα phosphorylation in a dose‑dependent manner, thereby preventing P65 from entering the nucleus, and resulting in inhibition of the NF‑κB signaling pathway. In addition, AC significantly reduced the expression of CDK4 and Cyclin D1 in a dose‑dependent manner, significantly upregulated the activation of caspase‑9 and caspase‑3, and decreased the Bcl‑2/Bax mRNA ratio. Furthermore, treatment with the NF‑κB signaling pathway inhibitor JSH‑23 significantly increased the cytotoxicity of AC in CRC cells. Findings of the xenograft mice model experiments revealed that AC significantly inhibited colorectal tumor growth in a dose‑dependent manner. Overall, AC suppressed activation of the NF‑κB signaling pathway by downregulating IκBα phosphorylation. This resulted in inhibition of CRC cell viability and an increase of cell apoptosis, which may form the basis of AC use in the treatment of patients with CRC.
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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.