Inhibitory effects of the ethanol extract of Gleditsia sinensis thorns on human colon cancer HCT116 cells in vitro and in vivo
- Authors
- Lee, Se-Jung; Cho, Young-Hwa; Kim, Heejong; Park, Keerang; Park, Sung-Kyu; Ha, Sang-Do; Kim, Wun-Jae; Moon, Sung-Kwon
- Issue Date
- Dec-2009
- Publisher
- SPANDIDOS PUBL LTD
- Keywords
- Gleditsia sinensis thorns; colon cancer; extracellular signal-regulated kinases; G2/M phase cell cycle arrest; p27; matrix metalloproteinase-9
- Citation
- ONCOLOGY REPORTS, v.22, no.6, pp 1505 - 1512
- Pages
- 8
- Journal Title
- ONCOLOGY REPORTS
- Volume
- 22
- Number
- 6
- Start Page
- 1505
- End Page
- 1512
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/22855
- DOI
- 10.3892/or_00000594
- ISSN
- 1021-335X
1791-2431
- Abstract
- The thorns of Gleditsia sinensis have traditionally been used in the treatment of several diseases, which includes their use as anti-tumor agents, but there has been no scientific evidence of this anti-tumor effect. However, the present study has identified a novel mechanism for the anti-tumor effect of Gleditsia sinensis thorns in the treatment of colon cancer. Treatment with the ethanol extract of Gleditsia sinensis thorns (EEGS) resulted in significant growth inhibition together with G2/M-phase cell cycle arrest at a dose of 600 mu g/ml (IC50) in HCT116 cells. In addition, treatment with EEGS induced p27 expression and down-regulated expression of cyclins and cyclin-dependent kinases. Moreover, EEGS treatment induced phosphorylation of extracellular signal-regulated kinases (ERK), p38 MAP kinase and JNK (c-Jun N-terminal kinases). Among the pathways examined, only PD98059 (ERK-specific inhibitor) abolished EEGS-dependent p27 expression. Similarly, suppression of ERK function reversed EEGS-mediated cell proliferation inhibition and decreased cell cycle proteins. In addition, tumor necrosis factor-alpha (TNF-alpha)-induced matrix metalloproteinase-9 (MMP-9) expression was inhibited by EEGS treatment via decreased transcriptional activity of both activator protein-1 (AP-1) and nuclear factor-kappa B. Finally, EEGS treatment significantly reduced tumor sizes in HCT116 cell-xenografted tumor tissues, which was associated with the changed levels of ERK phosphorylation, p27 and MMP-9 expression. Overall, these results have identified a novel molecular mechanism for EEGS in the treatment of colon cancer and might provide a theoretical basis for the potential therapeutic use of EEGS in the treatment of malignancies.
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