Context: The metastasis of liver cancer is a major cause of clinical treatment failure, restrain, and control the cancer metastasis is the major strategy of the treatment and prevention of the disease. Special AT-rich sequence-binding protein 1 (SATB1) gene was overexpressed in many malignant tumors and considered as a potential target of anticancer drug. This study investigated the mechanism how ganodermanontriol effect the expression of SATB1 and thus inhibits the growth and metastasis in hepatocellular carcinoma (HCC). Aims: This study explored mainly on the mechanism how ganodermanontriol affects the expression of SATB1 and inhibits proliferation of tumor on human hepatoma cell line HepG2. Settings and Design: The cancer cells were treated with ganodermanontriol. The status of the cells was detected by different methods. The mechanism was checked by various methods. Materials and Methods: In HepG2 cancer cells treated with various concentrations of ganodermanontriol, the cell proliferation of was detected by MTT assay, cell apoptosis was analyzed by flow cytometry; the mRNA of SATB1, Bcl-2, Bax were detected by reverse transcription-polymerase chain reaction (RT-PCR) and the protein level of SATB1, Bcl-2, Bax, and caspase 3 were analyzed by Western blot. Statistical Analysis Used: Data are presented as the mean ± standard deviation. The data were analyzed using SPSS 18.0 software (SPSS, Inc., Chicago, IL, USA) and GraphPad Prism software (GraphPad Software, Inc., La Jolla, CA, USA). A one-way analysis of variance test was used to compare the differences among groups. Results: This study showed that ganodermanontriol could significantly reduce the expression level of SATB1. Conclusion: Therefore, downregulate the cascade effect caused by the expression level of Bcl-2 in HCC HepG2 cells.
CITATION STYLE
Xu, C., Guo, H., Kong, D., Pang, D., & Ding, Y. (2018). Ganodermanontriol inhibits expression of special at rich sequence binding protein 1 gene in human hepatocellular carcinoma. Journal of Cancer Research and Therapeutics, 14(12), S964–S968. https://doi.org/10.4103/0973-1482.203597
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