Andrographolide Induces Apoptosis of C6 Glioma Cells via the ERK-p53-Caspase 7-PARP Pathway
Author(s) -
ShihHung Yang,
SeuMei Wang,
Jhih-Pu Syu,
Ying Chen,
ShengDe Wang,
YuSen Peng,
MengFai Kuo,
HsiuNi Kung
Publication year - 2014
Publication title -
biomed research international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 126
eISSN - 2314-6141
pISSN - 2314-6133
DOI - 10.1155/2014/312847
Subject(s) - andrographolide , apoptosis , glioma , in vivo , mapk/erk pathway , cancer research , poly adp ribose polymerase , andrographis paniculata , biology , flow cytometry , caspase , in vitro , signal transduction , chemistry , pharmacology , microbiology and biotechnology , programmed cell death , medicine , immunology , pathology , biochemistry , polymerase , alternative medicine , gene
Background. Glioma is the most malignant tumor of the central nervous system. Efforts on the development of new chemotherapy are mandatory. Andrographolide (AND), a diterpenoid lactone isolated from the Andrographis paniculata , has been shown to have antitumor activities in several types of cancer cells. Whether AND can exert its antitumor activity in glioblastoma cells remains unknown. This study examined the anticancer effects of AND, both in vitro and in vivo . Methods. Cell apoptosis was assayed by flow cytometry and nuclear staining. The signaling pathway for AND was determined by western blotting. The effects of AND on tumor growth was evaluated in a mouse model. Results and Conclusion. In vitro , with application of specific inhibitors and siRNA, AND-induced apoptosis was proven through ROS-ERK-P53-caspase 7-PARP signaling pathway. In vivo , AND significantly retarded tumor growth and caused regression of well-formed tumors in vivo . Furthermore, AND did not induce apoptosis or activate ERK and p53 in primary cultured astrocyte cells, and it may serve as a potential therapeutic candidate for the treatment of glioma.
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