Apoptosis induction and G2/M arrest of 2-methyl-1,3,6-trihydroxy-9,10-anthraquinone from Rubia yunnanensis in human cervical cancer Hela cells.

2-Methyl-1,3,6-trihydroxy-9,10-anthraquinone (MTA), one of the major components isolated from the traditional Chinese medicine Rubia yunnanensis, exhibited inhibitory activity on the proliferation of several human cancer cell lines. The results from an annexin V-FITC (fluoresein-5-isothiocyanate) apoptosis assay and DNA content analysis showed that MTA exerted cytotoxicity via apoptosis induction and G2/M cell cycle arrest in human cervical carcinoma HeLa cells. Further, MTA was found to induce apoptosis of HeLa cells through the mitochondria-mediated pathway. It caused the translocation of Bax to the mitochondria and release of cytochrome c into the cytosol, which caused the cleavage of caspase and poly(ADP-ribose) polymerase and finally triggered the apoptosis. Furthermore, the p53/p21/Cdc2-cyclin B1 signaling was found related to the G2/M arrest caused by MTA. The over-expression of p21 and down-expression of cyclin B1 caused by MTA inactivated the Cdc2-cyclin B1 complex of G2/M checkpoint and finally caused the G2/M arrest in HeLa cells. This study demonstrated that MTA is a potential anti-cancer component of R. yunnanensis, a folk anti-cancer herb used in Yunnan, China.