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Updated: Jan 21, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Diallyl disulfide inhibits colon cancer metastasis by suppressing Rac1-mediated epithelial-mesenchymal transition
Longzheng Xia1, Jingguan Lin1, Jian Su2
1Key Laboratory of Translational Radiation Oncology, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University and Hunan Cancer Hospital, Changsha 410013, Hunan, People's Republic of China.
Background:
Prevention of epithelial-mesenchymal transition (EMT) provides a novel treatment strategy for tumor metastasis. Our previous studies have shown that diallyl disulfide (DADS) inhibits Ras related C3 botulinum toxin substrate1 (Rac1) expression, being a potential agent that suppresses migration and invasion of colon cancer cells. The study provides information on the underlying mechanisms.
Methods:
The expression of Rac1 and EMT markers (vimentin, N-cadherin and E-cadherin) in colon cancer samples was detected. Colon cancer cell lines treated with or without DADS were used to examine EMT markers, Rac1 and its related molecules. Various cell functions related to metastasis were performed in vitro, and further confirmed in vivo.
Results:
Rac1 was highly expressed in colon cancer, and associated with aberrant expression of EMT markers and poor prognosis. Rac1 overexpression induced cell migration and invasion in vitro and metastasis in vivo with down-regulation of E-cadherin and up-regulation of N-cadherin, vimentin, and snail1, whereas inhibition of Rac1 impaired the oncogenic function. DADS suppressed Rac1 expression and activity via inhibition of PI3K/Akt pathway, thus suppressing EMT and invasion and migration of colon cancer cells. The tumor inhibition of DADS was enhanced by knockdown of Rac1, but antagonized by overexpression of Rac1. We further found that DADS blocked EMT via targeting the Rac1-mediated PAK1-LIMK1-Cofilins signaling.
Conclusion:
Rac1 is a potential target molecule for the inhibitory effect of DADS on EMT and invasion and metastasis of colon cancer cells.
Insights
Diallyl disulfide (DADS) suppresses colon cancer metastasis by inhibiting Rac1 expression and epithelial-mesenchymal transition (EMT). This study elucidates the molecular mechanisms underlying DADS
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Epithelial-mesenchymal transition (EMT) is a key driver of tumor metastasis, presenting a therapeutic target.
- Diallyl disulfide (DADS) has shown potential in suppressing colon cancer cell migration and invasion by inhibiting Ras related C3 botulinum toxin substrate1 (Rac1).
Purpose of the Study:
- To investigate the underlying mechanisms by which DADS inhibits Rac1 expression and its role in colon cancer metastasis.
- To explore Rac1 as a potential therapeutic target for colon cancer treatment.
Main Methods:
- Detection of Rac1 and EMT markers (vimentin, N-cadherin, E-cadherin) in colon cancer samples and cell lines.
- In vitro and in vivo assays to assess cell migration, invasion, and metastasis.
- Analysis of signaling pathways, including PI3K/Akt and Rac1-mediated PAK1-LIMK1-Cofilins.
Main Results:
- Rac1 overexpression correlates with aberrant EMT markers and poor prognosis in colon cancer.
- DADS suppresses Rac1 expression and activity by inhibiting the PI3K/Akt pathway, thereby reducing EMT, invasion, and migration.
- DADS blocks EMT through the Rac1-mediated PAK1-LIMK1-Cofilins signaling pathway.
Conclusions:
- Rac1 is a critical mediator of EMT, invasion, and metastasis in colon cancer.
- DADS effectively inhibits colon cancer progression by targeting Rac1 and its downstream signaling pathways.
- Rac1 represents a promising molecular target for DADS-based anti-cancer therapies.
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