The downregulation of c-Myc and its target gene hTERT is associated with the antiproliferative effects of baicalin on HL-60 cells.

Baicalin is a flavonoid compound isolated from Scutellaria baicalensis, a Chinese traditional medicinal herb, and is used as an anti-inflammatory, antibacterial, anxiolytic and hepatoprotective drug. Accumulating evidence has demonstrated that baicalin exhibits potent antitumor properties by suppressing cell growth, arresting cell cycle progression and inducing differentiation or apoptosis in leukemia cell lines. However, whether or not the extrinsic pathway is involved in baicalin-induced apoptosis of leukemia cells and the mechanisms underlying the antitumor activity of baicalin remain unclear. In the present study, the effect of baicalin on the expression of caspase-8, Fas cell surface death receptor (Fas) and Fas ligand in HL-60 cells was assessed, and it was demonstrated that the Fas-mediated extrinsic pathway was also involved in baicalin-triggered cell apoptosis, in addition to the intrinsic pathway. Furthermore, baicalin was able to inhibit the proliferation of HL-60 cells by arresting the cell cycle at the G0/G1 phase, and by down-regulating Myc proto-oncogene protein (c-Myc) along with its target gene, human telomerase reverse transcriptase. In summary, the results of the present study demonstrated that baicalin was able to inhibit the growth of HL-60 cells through blockade of the G0/G1 phase of the cell cycle, and significantly induce the apoptosis of cells by activating the intrinsic and extrinsic pathways. The inhibition of HL-60 cell growth was also demonstrated to be mediated by telomerase inhibition through suppression of c-Myc. The results of the present study highlight the possibility of baicalin as a promising regimen for the treatment of AML.