Baicalin induces cell cycle arrest and apoptosis of human colon cancer in vitro and in vivo
10.3781/j.issn.1000-7431.2017.11.716
- Author:
Huiru BAI
1
Author Information
1. Jiangsu Key Laboratory for Molecular and Medical Biotechnology, School of Life Sciences, Nanjing Normal University
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Baicalin;
Cell cycle;
Colonic neoplasms;
Xenograft model antitumor assays
- From:
Tumor
2017;37(3):208-217
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effects of baicalin on the cell cycle and apoptosis of human colon cancer in vitro and in vivo, and to further clarify its possible molecular mechanism. Methods: After treatment with different concentrations (0, 50, 100, 200, 400 and 800 μg/mL) of baicalin for 48 h, the morphology and viability of human normal colorectal mucosa FHC cells and human colon cancer HCT116 cells were detected by invert microscopy and MTT method, respectively. The changes of apoptosis rate and cell cycle distribution of HCT116 cells after baicalin treatment were detected by flow cytometry. The expression levels of apoptosis-related proteins [poly ADP-ribose polymerase-1 (Parp-1), caspase 3, X-linked inhibitor of apoptosis protein (XIAP), nuclear factor-κB (NF-κB), p53, Bcl-2 and Bax] and cell cycle-related proteins (cyclin D1 and cyclin B1) in HCT116 cells treated with baicalin were measured by Western blotting. After the orthotopic xenograft tumor model of colon cancer HCT116 cells in nude mice were constructed and treated with baicalin by gavage, the body weight of mice and the tumor size were checked, and the baicalin-induced apoptosis in xenograft tumors was also assayed using TUNEL methods. Results: As compared with baicalin-untreated control group, 50-800 μg/mL baicalin significantly suppressed the viability of colon cancer HCT116 cells (all P < 0.05). The half maximal inhibitory concentration (IC50) of baicalin in the normal colorectal mucosa FHC cells was significantly higher than that in colon cancer HCT116 cells (P < 0.01). After treatment with 200 and 400 μg/mL baicalin, the apoptosis rate of HCT116 cells was significantly increased (both P < 0.01). After treatment with 50 and 100 μg/mL baicalin for 48 h, the expression levels of cleaved-Parp-1 and cleaved-caspase 3 proteins were significantly up-regulated (all P < 0.01), while the expression levels of XIAP, NF-κB and Bcl-2 protein were significantly down-regulated (all P < 0.05). Furthermore, after treatment with 100 and 200 μg/mL baicalin, HCT116 cell cycle arrested at G1 phase (both P < 0.01). After treatment with 50 and 100 μg/mL baicalin for 48 h, the levels of cyclin D1 and cyclin B1 proteins in HCT116 cells were significantly downregulated (all P < 0.01). Additionally, baicalin significantly inhibited the growth of xenograft tumors in mice (P < 0.01), and promoted the apoptosis of tumor cells in vivo, but had no obvious effect on the body weight of mice (P > 0.05). Conclusion: Baicalin can inhibit the growth of colon cancer HCT116 cells in vivo and in vitro through inducing apoptosis and cell cycle arrest at G1 phase.
