Artesunate inhibits proliferation of glioblastoma cells by arresting cell cycle.
10.19540/j.cnki.cjcmm.20171121.002
- Author:
Xiong WENG
1
;
Shun-Qin ZHU
2
;
Hong-Juan CUI
1
Author Information
1. State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, China.
2. School of Life Sciences， Southwest University， Chongqing 400715, China.
- Publication Type:Journal Article
- Keywords:
artesunate;
cell cycle;
glioblastoma;
proliferation
- MeSH:
Antineoplastic Agents;
pharmacology;
Apoptosis;
Artesunate;
pharmacology;
Cell Cycle Checkpoints;
drug effects;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Cyclin B1;
metabolism;
Cyclin D1;
metabolism;
Cyclin-Dependent Kinase 2;
metabolism;
Cyclin-Dependent Kinase 4;
metabolism;
Glioblastoma;
drug therapy;
pathology;
Humans
- From:
China Journal of Chinese Materia Medica
2018;43(4):772-778
- CountryChina
- Language:Chinese
-
Abstract:
Glioblastoma is a common brain tumor and the overall survival rate of the patients is very low, so it is an effective way to develop the potential chemotherapy or adjuvant chemotherapy drugs in glioblastoma treatment. As a well-known antimalarial drug, artesunate(ARTs) has clear side effects, and recently it has been reported to have antitumor effects, but rarely reported in glioblastoma. Different concentrations of ARTs were used to treat the glioblastoma cells, and then the inhibitory effect of ARTs on glioblastoma proliferation was detected by MTT assay; Ki67 immunofluorescence assay was used to detect the proliferation of cells; Soft agar experiment was used to explain the clonal formation abilities ; Flow Cytometry was used to detect the cell cycle; and Western blot assay was used to determine the expression of key cell cycle protein. MTT assay results indicated that ARTs-treated glioblastoma cell A172, U251, U87 were significantly inhibited in a time-and-dose dependent manner as compared to the control group(DMSO treatment group). Soft agar experiment showed that ARTs could significantly reduce the clonal formation ability of glioblastoma. Furthermore, Flow cytometry analysis showed that ARTs could obviously increase the cell proportion in G₀/G₁ phase and reduce the cell proportion in S phase. Western blot results showed that the expressions of cell cycle-related proteins CDK2, CDK4, cyclin D1 and cyclin B1 were all obviously down-regulated. Above all, ARTs may inhibit the proliferation of glioblastoma cells by arresting cell cycle in G₀/G₁ phase through down-regulating the expression of CDK2, CDK4, cyclin D1, cyclin B1. These results may not only provide a novel method for rediscovering and reusing ARTs but also provide a new potential drug for treating glioblastoma.
