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Oncotarget. 2016 Mar 1;7(9):10498-512. doi: 10.18632/oncotarget.7252.

Diallyl disulfide suppresses epithelial-mesenchymal transition, invasion and proliferation by downregulation of LIMK1 in gastric cancer.

Su B1,2,3, Su J1,2,4, Zeng Y1,2, Liu F1,2, Xia H1,2, Ma YH1,2, Zhou ZG1,2, Zhang S1,2, Yang BM1,2, Wu YH1, Zeng X1,2, Ai XH1, Ling H1,2, Jiang H1, Su Q1,2.

Author information

Center for Gastric Cancer Research of Hunan Province, First Affiliated Hospital, University of South China, Hengyang, 421001 Hunan, China.
Key Laboratory of Cancer Cellular and Molecular Pathology of Hunan Provincial University, Cancer Research Institute, University of South China, Hengyang, 421001 Hunan, China.
Key Laboratory for Pharmacoproteomics of Hunan Provincial University, Institute of Pharmacy and Pharmacology, University of South China, Hengyang, 421001 Hunan, China.
Department of Pathology, Second Affiliated Hospital, University of South China, Hengyang, 421001 Hunan, China.


Diallyl disulfide (DADS) has been shown to have multi-targeted antitumor activities. We have previously discovered that it has a repressive effect on LIM kinase-1 (LIMK1) expression in gastric cancer MGC803 cells. This suggests that DADS may inhibit epithelial-mesenchymal transition (EMT) by downregulating LIMK1, resulting in the inhibition of invasion and growth in gastric cancer. In this study, we reveal that LIMK1 expression is correlated with tumor differentiation, invasion depth, clinical stage, lymph node metastasis, and poor prognosis. DADS downregulated the Rac1-Pak1/Rock1-LIMK1 pathway in MGC803 cells, as shown by decreased p-LIMK1 and p-cofilin1 levels, and suppressed cell migration and invasion. Knockdown and overexpression experiments performed in vitro demonstrated that downregulating LIMK1 with DADS resulted in restrained EMT that was coupled with decreased matrix metalloproteinase-9 (MMP-9) and increased tissue inhibitor of metalloproteinase-3 (TIMP-3) expression. In in vitro and in vivo experiments, the DADS-induced suppression of cell proliferation was enhanced and antagonized by the knockdown and overexpression of LIMK1, respectively. Similar results were observed for DADS-induced changes in the expression of vimentin, CD34, Ki-67, and E-cadherin in xenografted tumors. These results indicate that downregulation of LIMK1 by DADS could explain the inhibition of EMT, invasion and proliferation in gastric cancer cells.


LIMK1; diallyl disulfide; gastric cancer cell epithelial-mesenchymal transition; invasion; proliferation

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