ArticleCell research2011
Slit-Robo signaling induces malignant transformation through Hakai-mediated E-cadherin degradation during colorectal epithelial cell carcinogenesis.
Article in Cell research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 89 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
89 citing papers in PubMed, 134 citations in OpenAlex.
- E3 ubiquitin-ligase Hakai regulates LRP4 stability and Wnt/β-catenin signalling in colorectal cancer cells.iScience · 2026Article
- Development and validation of a 5mC-based prognostic model for lung adenocarcinoma survival.Cell reports. Medicine · 2026Article
- Activation of SLIT2/ROBO1/LRP6 axis aggravates cartilage degradation via β-catenin signaling in TMJOA.JCI insight · 2026Article
- Frizzled-1 amplification promotes fibrosis in the gastric tumor microenvironment through the activation of fibroblasts via the SLIT2/ROBO1 axis.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026Article
- The role of deubiquitinase USP33 in colorectal cancer tumorigenesis and its potential as a therapeutic target predictor.Discover oncology · 2026Review
- Discovery of a first-in-class SLIT2 binder disrupting the SLIT2/ROBO1 axisRSC medicinal chemistry · 2025Article
- PIEZO2 in tumors: from mechanobiological switches to activity-targeted therapies.Journal of experimental & clinical cancer research : CR · 2025Review
- Optimization and development of a high-throughput TR-FRET screening assay for SLIT2/ROBO1 interaction.SLAS discovery : advancing life sciences R & D · 2025Article
- Tailoring a novel colorectal cancer stem cell-targeted therapy by inhibiting the SMYD3/c-MYC axis.Signal transduction and targeted therapy · 2025Article
- Neuronal mimicry in tumors: lessons from neuroscience to tackle cancer.Cancer metastasis reviews · 2025Review
- Beyond destruction: emerging roles of the E3 ubiquitin ligase Hakai.Cellular & molecular biology letters · 2025Review
- Traditional Chinese medicine for breast cancer treatment: a bibliometric and visualization analysis.Pharmaceutical biology · 2024Review
- Multiomics integration-based immunological characterizations of adamantinomatous craniopharyngioma in relation to keratinization.Cell death & disease · 2024Article
- Anti-Cancer Mechanisms of Diarylpentanoid MS17 (1,5-Bis(2-hydroxyphenyl)-1,4-pentadiene-3-one) in Human Colon Cancer Cells: A Proteomics Approach.International journal of molecular sciences · 2024Article
- Involvement of neuronal factors in tumor angiogenesis and the shaping of the cancer microenvironment.Frontiers in immunology · 2024Review
- SLIT3 deficiency promotes non-small cell lung cancer progression by modulating UBE2C/WNT signaling.Open life sciences · 2024Article
- Article
- LINC01343 targets miR-526b-5p to facilitate the development of hepatocellular carcinoma by upregulating ROBO1.Scientific reports · 2023Article
- SLIT2/ROBO1 signaling suppresses mTORC1 for organelle control and bacterial killing.Life science alliance · 2023Article
- Genome-wide CRISPR knockout screening identified G protein pathway suppressor 2 as a novel tumor suppressor for uveal melanoma metastasis.Journal of cancer research and clinical oncology · 2023Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
Abstract
The Slit family of guidance cues binds to Roundabout (Robo) receptors and modulates cell migration. We report here that ectopic expression of Slit2 and Robo1 or recombinant Slit2 treatment of Robo1-expressing colorectal epithelial carcinoma cells recruited an ubiquitin ligase Hakai for E-cadherin (E-cad) ubiquitination and lysosomal degradation, epithelial-mesenchymal transition (EMT), and tumor growth and liver metastasis, which were rescued by knockdown of Hakai. In contrast, knockdown of endogenous Robo1 or specific blockade of Slit2 binding to Robo1 prevented E-cad degradation and reversed EMT, resulting in diminished tumor growth and liver metastasis. Ectopic expression of Robo1 also triggered a malignant transformation in Slit2-positive human embryonic kidney 293 cells. Importantly, the expression of Slit2 and Robo1 was significantly associated with an increased metastatic risk and poorer overall survival in colorectal carcinoma patients. We conclude that engagement of Robo1 by Slit2 induces malignant transformation through Hakai-mediated E-cad ubiquitination and lysosomal degradation during colorectal epithelial cell carcinogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.