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Updated: Apr 18, 2026

In vitro Organoid Culture of Primary Mouse Colon Tumors
Published on: May 17, 2013
Slit2/Robo1 signaling promotes intestinal tumorigenesis through Src-mediated activation of the Wnt/β-catenin pathway
Qian-Qian Zhang1, Da-Lei Zhou1, Yan Lei1
1Vascular Biology Research Institute, Guangdong Pharmaceutical University, Guangzhou, China.
Abstract:
Slit2 is often overexpressed in cancers. Slit2 is a secreted protein that binds to Roundabout (Robo) receptors to regulate cell growth and migration. Here, we employed several complementary mouse models of intestinal cancers, including the Slit2 transgenic mice, the ApcMin/+ spontaneous intestinal adenoma mouse model, and the DMH/DSS-induced colorectal carcinoma model to clarify function of Slit2/Robo1 signaling in intestinal tumorigenesis. We showed that Slit2 and Robo1 are overexpressed in intestinal tumors and may contribute to tumor generation. The Slit2/Robo1 signaling can induce precancerous lesions of the intestine and tumor progression. Ectopic expression of Slit2 activated Slit2/Robo1 signaling and promoted tumorigenesis and tumor growth. This was mediated in part through activation of the Src signaling, which then down-regulated E-cadherin, thereby activating Wnt/β-catenin signaling. Thus, Slit2/Robo1 signaling is oncogenic in intestinal tumorigenesis.
Insights
Slit2 and Robo1 are overexpressed in intestinal tumors, promoting cancer growth and progression. This signaling pathway activates Src and Wnt/β-catenin, driving tumorigenesis.
Area of Science:
- Oncology
- Molecular Biology
- Cell Signaling
Background:
- Slit2 is a secreted protein involved in cell growth and migration.
- Slit2 functions by binding to Roundabout (Robo) receptors.
- Overexpression of Slit2 is observed in various cancers.
Purpose of the Study:
- To investigate the role of Slit2/Robo1 signaling in intestinal tumorigenesis.
- To elucidate the mechanisms by which Slit2/Robo1 signaling influences tumor development.
Main Methods:
- Utilized multiple mouse models of intestinal cancer: Slit2 transgenic, ApcMin/+, and DMH/DSS-induced colorectal carcinoma models.
- Analyzed the expression of Slit2 and Robo1 in intestinal tumors.
- Investigated the downstream signaling pathways activated by Slit2/Robo1.
Main Results:
- Slit2 and Robo1 were found to be overexpressed in intestinal tumors.
- Slit2/Robo1 signaling was shown to induce precancerous intestinal lesions and promote tumor progression.
- Ectopic Slit2 expression enhanced tumorigenesis and tumor growth.
- Slit2/Robo1 signaling activated Src signaling, leading to E-cadherin downregulation and Wnt/β-catenin activation.
Conclusions:
- Slit2/Robo1 signaling plays an oncogenic role in intestinal tumorigenesis.
- The Slit2/Robo1 pathway contributes to tumor generation and progression through Src and Wnt/β-catenin signaling.
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