ArticleHeliyon2024
Allicin affects immunoreactivity of osteosarcoma cells through lncRNA CBR3-AS1.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Allicin inhibits colon cancer cells biological activity by regulating lncRNA UCA1 via autophagy stimulating.Discover oncology · 2026Article
- Role of miRNA‑145‑5p in cancer (Review).Oncology reports · 2025Review
- Cuproptosis related lncRNA signature as a prognostic and therapeutic biomarker in osteosarcoma immunity.Scientific reports · 2025Article
- Discovery of drug transporter inhibitors tied to long noncoding RNA in resistant cancer cells; a computational model -in silico- study.Frontiers in immunology · 2025Review
- Mini-review: The health benefits and applications of allicin.Frontiers in pharmacology · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: To analyze the effect of allicin on the immunoreactivity of osteosarcoma (OS) cells and further explore whether its mechanism is related to the long non-coding Ribonucleic Acid (lncRNA) CBR3-AS1/miR-145-5p/GRP78 axis, so as to provide clinical evidence. Methods: The human OS cell line Saos-2 was treated with allicin at 25, 50, and 100 μmol/L, respectively, to observe changes in cell biological behaviors. Subsequently, CBR3-AS1 abnormal expression vectors were constructed and transfected into Saos-2 to discuss their influence on OS. Furthermore, the regulatory relationship between allicin and the CBR3-AS1/miR-145-5p/GRP78 axis was validated by rescue experiments. Finally, a nude mice tumorigenesis experiment was carried out to analyze the effects of allicin and CBR3-AS1/miR-145-5p/GRP78 axis on the growth of living tumors. Alterations in T-lymphocyte subsets were also detected to assess the effect of allicin on OS immunoreactivity. Results: With the increase of allicin concentration, Saos-2 activity decreased and apoptosis increased (P < 0.05). In addition, the expression of CBR3-AS1 and GRP78 decreased after allicin intervention, while miR-145-5p increased (P < 0.05). Silencing CBR3-AS1 led to reduced Saos-2 activity, enhanced apoptosis, and activated mitophagy and endoplasmic reticulum stress (P < 0.05). In the rescue experiment, the effect of CBR3-AS1 on OS cells was reversed by silencing miR-145-5p, while the impact of miR-145-5p was reversed by GRP78. Finally, the tumorigenesis experiment in nude mice confirmed the regulatory effects of allicin and CBR3-AS1/miR-145-5p/GRP78 on tumor growth in vivo. Meanwhile, it was seen that allicin activated CD4 Conclusions: Allicin activates OS immunoreactivity and induces apoptosis through the CBR3-AS1/miR-145-5p/GRP78 molecular axis.
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