Baicalin is a major component of PC-SPES which inhibits the proliferation of human cancer cells via apoptosis and cell cycle arrest

BACKGROUND. PC-SPES is an eight-herb mixture that was shown to have activit y against Prostate cancer. Recently, we isolated a major component (6% of t he total ethanolic extract) known as baicalin from PC-SPES by high performa nce liquid chromatography (HPLC). METHODS. Baicalin was evaluated for its ability to inhibit clonal growth, a nd to induce cell cycle arrest of various cancer types (PC-3, DU145, LNCaP prostate cancer cell lines, MCF-7 breast cancer cell line, HL-60 myeloblast ic leukemia cell line, and NB4 promyelocytic leukemia cell line). The abili ty of baicalin to induce apoptosis of cancer cells was examined by both sta ining with Annexin V and detection of cleavage of Poly (ADP-ribose) polymer ase (PARP)(3). Western blot analysis examined the effect of baicalin on lev els of p2(waf1) and p27(kip1) in those cells. Futhermore, induction of diff erentiation in HL-60 cells was measured by expression of CD11b. RESULTS. Baicalin inhibited the clonal proliferation of LNCaP and PC3 prost ate cancer cell lines, and the HL-60 and NB4 myeloblastic/promyelocytic leu kemia cell lines with a 50% inhibition (ED50) that ranged between 6.4 x 10( -6) to 12 x 10(-6) mol/L. Cell cycle analysis showed that baicalin (2 x 10( -5) mol/L, 4 days) caused a G(0)/G(1) and G(2)/M accumulation of LNCaP and HL-60 cells, respectively. Concomitantly, differentiation and apoptosis wer e induced in HL-60 cells, as measured by expression of CD11b antigen, stain ing with annexin V, and detection of cleavage of PARP. Moreover, baicalin e nhanced the expression of the cyclin-dependent kinase inhibitor, p27(kip1) in LNCaP and HL-60 cells. CONCLUSIONS. Baicalin inhibited the proliferation of cancer cells via apopt osis and cell cycle arrest, in which p27(kip1) may play a role. Baicalin ma y be a novel, adjunctive therapy for selected malignancies including prosta te cancer. (C) 2001 Wiley-Liss, Inc.