Methylsulfonylmethane suppresses hepatic tumor development through activation of apoptosis

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Title
Methylsulfonylmethane suppresses hepatic tumor development through activation of apoptosis
Author(s)
Joo Hyun Kim; Hye Jun Shin; H L Ha; Young-Ho ParkTaeho Kwon; Mi Ra Jung; H B Moon; E S Cho; H Y Son; Dae Yeul Yu
Bibliographic Citation
World Journal of Hepatology, vol. 6, no. 2, pp. 98-106
Publication Year
2014
Abstract
Aim: To investigate the effect of methylsulfonylmethane (MSM), recently reported to have anti-cancer effects, in liver cancer cells and transgenic mice. Methods: Three liver cancer cell lines, HepG2, Huh7-Mock and Huh7-H-rasG12V, were used. Cell growth was measured by Cell Counting Kit-8 and soft agar assay. Western blot analysis was used to detect caspases, poly (ADP-ribose) polymerase (PARP), and B-cell lymphoma 2 (Bcl-2) expressions. For in vivo study, we administered MSM to H-ras12V transgenic mice for 3 mo. Results: MSM decreased the growth of HepG2, Huh7-Mock and Huh7-H-rasG12V cells in a dose-dependent manner. That was correlated with significantly increased apoptosis and reduced cell numbers in MSM treated cells. Cleaved caspase-8, cleaved caspase-3 and cleaved PARP were remarkably increased in the liver cancer cells treated with 500 mmol/L of MSM; however, Bcl-2 was slightly decreased in 500 mmol/L. Liver tumor development was greatly inhibited in the H-ras12V transgenic mice treated with MSM, compared to control, by showing reduced tumor size and number. Cleaved PARP was significantly increased in non-tumor treated with MSM compared to control. Conclusion: Liver injury was also significantly attenuated in the mice treated with MSM. Taken together, all the results suggest that MSM has anti-cancer effects through inducing apoptosis in liver cancer.
Keyword
Anti-cancer effectsHepatic tumorigenesisLiver cancer cellsMethylsulfonylmethaneTransgenic mice
ISSN
1948-5182
Publisher
Baishideng Publishing Group
DOI
http://dx.doi.org/10.4254/wjh.v6.i2.98
Type
Article
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Futuristic Animal Resource & Research Center > 1. Journal Articles
Jeonbuk Branch Institute > Primate Resources Center > 1. Journal Articles
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