Abstract Title:

[Experimental study on anti-metastasis effect of emodin on human pancreatic cancer].

Abstract Source:

Zhongguo Zhong Yao Za Zhi. 2011 Nov ;36(22):3167-71. PMID: 22375400

Abstract Author(s):

An Liu, Lixiao Sha, Yue Shen, Lili Huang, Xiao Tang, Shengzhang Lin

Article Affiliation:

First People Hospital of Yueyang, Yueyang 414000, China. [email protected]

Abstract:

OBJECTIVE: To investigate the anti-metastasis effect of emodin on the pancreatic cancer in vitro and in vivo.

METHOD: Human pancreatic cancer cell line SW1990 was treated with different concentrations of emodin (10, 20, 40 micromol x L(-1)) for 2 h, the effects of emodin on the migration and invasion of SW1990 cells were examined by using wound assay and matrigel counting. Western blot was used to detect the protein expression of NF-kappaB and MMP-9 in SW1990 cells after various concentrations of emodin (10, 20, 40 micromol x L(-1)) treatment for 48 h. Metastatic model simulating human pancreatic cancer was established by orthotropic implantation of histologically intact human tumor tissue into pancreatic wall of nude mice, and then divided into three groups: control group, low-dose emodin group (L-EMO) and high-dose emodin group (H-EMO). Eight weeks after implantation, the presences of metastasis were evaluated respectively after the mice were sacrificed. Immunohistochemistry was used to detect the positive expression of CD34, NF-kappaB and MMP-9 in the tumors.

RESULT: Emodin suppressed the migration and invasion of SW1990 cells in a dose-dependent manner. Western bolt assay indicated that emodin down-regulated the expression of NF-kappaB and MMP-9 proteins in SW1990 cells. The incidences of metastasis were decreased significantly in L-EMO group and H-EMO group as compared with that in control group. The percentage of CD34, NF-kappaB and MMP-9-positive cells in the tumors were significantly reduced by the administration of emodin.

CONCLUSION: Emodin exerts anti-metastatic activity in pancreatic cancer both in vitro and in vivo, which may be related to down-regulation of NF-kappaB and MMP-9.

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