Lycorine inhibits the proliferation of acute myeloid leukemia cells by upregulating the expression of THBS1.

To clarify the biological roles of the putative target thrombospondin-1 (THBS1) and the impact of the traditional Chinese medicine monomer Lycorine on acute myeloid leukemia (AML) cells. The AML cell lines HL-60 and THP-1 were used in vitro to assess the effects of lycorine on cell growth and apoptosis. Network pharmacology and Gene Expression Omnibus (GEO) database analysis were used to predict potential lycorine targets in AML. Clinical samples were used to validate the target THBS1's expression. The binding affinity between lycorine and THBS1 was examined using molecular docking. Lastly, THBS1 overexpression in AML cells confirmed its function. In a dose-dependent way, lycorine induced apoptosis and markedly suppressed the growth of AML cell lines. THBS1 is a common target of lycorine in AML, and its expression is dramatically downregulated in AML, according to network pharmacology, GEO database analysis, and confirmation using clinical samples. Lycorine's ability to bind to THBS1 and increase its expression levels in AML cells was validated by molecular docking. In AML cells, THBS1 overexpression mirrored the effects of lycorine by preventing cell division and triggering apoptosis. Lycorine inhibits the growth of AML cells and triggers apoptosis by targeting and upregulating the expression of THBS1. Therefore, it has antileukemic actions. One of the main targets for anti-AML treatment is THBS1.