Premium
Baicalin is a major component of PC‐SPES which inhibits the proliferation of human cancer cells via apoptosis and cell cycle arrest
Author(s) -
Ikezoe Takayuki,
Chen Sophie S.,
Heber David,
Taguchi Hirokuni,
Koeffler H. Phillip
Publication year - 2001
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.10024
Subject(s) - baicalin , lncap , acute promyelocytic leukemia , cell cycle , apoptosis , cell growth , cell culture , cancer cell , annexin , microbiology and biotechnology , biology , du145 , cancer research , chemistry , cancer , biochemistry , retinoic acid , high performance liquid chromatography , chromatography , genetics
Background PC‐SPES is an eight‐herb mixture that was shown to have activity against prostate cancer. Recently, we isolated a major component (6% of the total ethanolic extract) known as baicalin from PC‐SPES by high performance liquid chromatography (HPLC). Methods Baicalin was evaluated for its ability to inhibit clonal growth, and 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 myeloblastic leukemia cell line, and NB4 promyelocytic leukemia cell line). The ability of baicalin to induce apoptosis of cancer cells was examined by both staining with Annexin V and detection of cleavage of Poly (ADP‐ribose) polymerase (PARP) 3 . Western blot analysis examined the effect of baicalin on levels of p21 waf1 and p27 kip1 in those cells. Futhermore, induction of differentiation in HL‐60 cells was measured by expression of CD11b. Results Baicalin inhibited the clonal proliferation of LNCaP and PC3 prostate cancer cell lines, and the HL‐60 and NB4 myeloblastic/promyelocytic leukemia cell lines with a 50% inhibition (ED 50 ) that ranged between 6.4 × 10 −6 to 12 × 10 −6 mol/L. Cell cycle analysis showed that baicalin (2 × 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 were induced in HL‐60 cells, as measured by expression of CD11b antigen, staining with annexin V, and detection of cleavage of PARP. Moreover, baicalin enhanced 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 apoptosis and cell cycle arrest, in which p27 kip1 may play a role. Baicalin may be a novel, adjunctive therapy for selected malignancies including prostate cancer. Prostate 49:285–292, 2001. © 2001 Wiley‐Liss, Inc.