ArticleDiscover oncology2026
Allicin inhibits colon cancer cells biological activity by regulating lncRNA UCA1 via autophagy stimulating.
Article in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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8 authors.
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Abstract
objectiveThis study aimed to investigate the mechanism by which allicin, a bioactive compound from garlic, exerts antitumor effects, specifically focusing on its role in regulating the long non-coding RNA UCA1 via the induction of autophagy.
methodsExperiments were conducted using human colorectal cancer cell lines HCT-116 and HT-29. Cell proliferation was measured with a CCK-8 kit, apoptosis was analyzed by flow cytometry, cell invasion was assessed using Transwell chambers, and migration was evaluated via a scratch wound assay. Autophagic structures were examined under a transmission electron microscope. The expression level of lncRNA UCA1 was determined by quantitative reverse transcription polymerase chain reaction (RT-qPCR), and the expression of proteins associated with autophagy was detected by western blot analysis.
resultsCompared with the control group, allicin treatment significantly inhibited cancer cell proliferation, increased the rate of apoptosis, and reduced capabilities for invasion and migration. Furthermore, allicin downregulated the expression of lncRNA UCA1 in a concentration-dependent manner and simultaneously increased the number of autophagosomes. All these effects were statistically significant (P < 0.05). However, when cells were co-treated with an mTOR activator, the antitumor effects of allicin and the increase in autophagosomes were significantly counteracted (P < 0.001).
conclusionAllicin inhibited colon cancer cell activities through the induction of cellular autophagy and the subsequent regulation of lncRNA UCA1 expression.
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