Induction of apoptosis in human glioma cell lines of various grades through the ROS-mediated mitochondrial pathway and caspase activation by Rhaponticum carthamoides transformed root extract

The present study is the first investigation of the inhibitory effect of Rhaponticum carthamoides transformed roots (TR) extract on the proliferation of grade II and III human glioma cells. TR extract showed the cytotoxic effect and inhibited the colony formation of both glioma cell lines in dose-de...

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Published in:Molecular and cellular biochemistry 2018-08, Vol.445 (1-2), p.89-97
Main Authors: Skała, Ewa, Kowalczyk, Tomasz, Toma, Monika, Szemraj, Janusz, Radek, Maciej, Pytel, Dariusz, Wieczfinska, Joanna, Wysokińska, Halina, Śliwiński, Tomasz, Sitarek, Przemysław
Format: Article
Language:English
Subjects:
Anticancer properties
Antitumor activity
Apoptosis
Biochemistry
Biomedical and Life Sciences
Biotechnology
Brain tumors
Cancer
Cardiology
Caspase
Caspase-3
Caspase-9
Cell death
Cell lines
Cell proliferation
Cells
Cytotoxicity
Extraction processes
Glioma
Glioma cells
Gliomas
Life Sciences
Medical Biochemistry
Membrane potential
Mitochondria
mRNA
Oncology
p53 Protein
Reactive oxygen species
RNA
Tumor proteins
Tumors
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Summary:The present study is the first investigation of the inhibitory effect of Rhaponticum carthamoides transformed roots (TR) extract on the proliferation of grade II and III human glioma cells. TR extract showed the cytotoxic effect and inhibited the colony formation of both glioma cell lines in dose-dependent manner. The root extract induced apoptosis by increasing of the reactive oxygen species (about threefold compared to the control cells) leading to a disruption of mitochondrial membrane potential. Additionally, the mRNA levels of the apoptotic factors such as Bax, Tp53, caspase-3, and caspase-9 were observed to increase. These results indicate that the TR extract possesses anticancer activity by inhibiting glioma cell proliferation and inducing apoptotic cell death, and may be used as a promising anticancer agent.
ISSN:0300-8177
1573-4919
DOI:10.1007/s11010-017-3254-z