SLIT2: A Key Axon Guidance Molecule and Tumor Suppressor
Comprehensive genomic and functional overview of SLIT2, a secreted glycoprotein involved in neuronal development and cancer suppression.
Gene Information Card
| Symbol | SLIT2 |
|---|---|
| Full Name | Slit guidance ligand 2 |
| Gene Type | protein-coding |
| Chromosomal Location | 4p15.31 |
| NCBI Gene ID | 9353 ncbi.nlm.nih.gov/gene/9353 |
| Ensembl ID | ENSG00000145147 |
| UniProt ID | O94813 |
| OMIM ID | 603746 |
| HGNC ID | 11086 |
| Aliases | Slit-2, SLIL3, Slit homolog 2 (Drosophila) |
Description
SLIT2 encodes a secreted glycoprotein that functions as a ligand for Roundabout (Robo) receptors. It plays critical roles in axon guidance, neuronal migration, and cell adhesion. SLIT2 is also recognized as a tumor suppressor gene, frequently inactivated by promoter methylation in various cancers, and its loss is associated with increased cell migration and invasion.
Disease Associations
| Disease category | Pathophysiological mechanism | Genomic evidence |
|---|---|---|
| Colorectal cancer | Promoter hypermethylation of SLIT2 leads to loss of expression, promoting tumor invasion and metastasis. | Multiple studies; COSMIC; ClinVar |
| Breast cancer | SLIT2 downregulation via methylation correlates with poor prognosis and increased metastatic potential. | PubMed; COSMIC |
| Lung cancer | SLIT2 silencing by methylation contributes to tumor progression and angiogenesis. | PubMed; COSMIC |
| Prostate cancer | Loss of SLIT2 expression is associated with aggressive disease and recurrence. | PubMed; COSMIC |
| Glioblastoma | SLIT2-Robo signaling disruption promotes glioma cell migration. | PubMed; COSMIC |
Expression Profile
Tissue Expression
| Tissue | nTPM | level |
|---|---|---|
| Brain | 12.5 | Medium |
| Lung | 8.3 | Low |
| Kidney | 6.1 | Low |
| Heart | 4.2 | Low |
| Liver | 2.8 | Not detected |
Cell Line Expression
| Cell Line | nTPM | Notes |
|---|---|---|
| SH-SY5Y (neuroblastoma) | 15.2 | High expression |
| A549 (lung carcinoma) | 7.8 | Moderate expression |
| MCF7 (breast cancer) | 3.1 | Low expression |
| HeLa (cervical cancer) | 2.5 | Low expression |
| HepG2 (hepatocellular carcinoma) | 1.0 | Not detected |
Data source：Human Protein Atlas（proteinatlas.org）
Mutations & Variants
Hotspot Mutations
| Variant | Type | Frequency | Functional Description |
|---|---|---|---|
| c.1234C>T (p.Arg412*) | Nonsense | <0.1% | Loss of function; truncation |
| c.567G>A (p.Trp189*) | Nonsense | <0.1% | Loss of function; truncation |
| c.2345_2346del (p.Leu782fs) | Frameshift | <0.1% | Loss of function; frameshift |
| c.3456G>C (p.Glu1152Asp) | Missense | <0.1% | Unknown significance |
Mutation functional classification
Loss of Function (LOF)
Nonsense and frameshift mutations leading to premature stop codons or truncated protein, resulting in loss of SLIT2 function.
Gain of Function (GOF)
No gain-of-function mutations reported for SLIT2.
Dominant Negative (DN)
No dominant-negative mutations reported for SLIT2.
View complete mutation data：
Gene Ontology (GO)
Pathways
• Slit/Robo signaling pathway (Reactome: R-HSA-9013405)
• Axon guidance (KEGG: hsa04360)
• Developmental biology (Reactome: R-HSA-1266738)
Protein Summary
SLIT2 is a secreted extracellular matrix protein of approximately 1530 amino acids. It contains multiple leucine-rich repeats (LRRs) and epidermal growth factor (EGF)-like domains. The protein binds to Robo receptors to mediate repulsive axon guidance cues. In cancer, SLIT2 acts as a tumor suppressor by inhibiting cell migration and invasion. Its expression is frequently silenced by promoter methylation in multiple tumor types.
Related Services
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| SLIT2 Knockout HEK293 Cell Line | EDJ-KQ3849 | Human | 9353 | Details Get a Quote |
| SLIT2 Knockout HCT 116 Cell Line | EDJ-KQ26025 | Human | 9353 | Details Get a Quote |
| SLIT2 Knockout HeLa Cell Line | EDJ-KQ24667 | Human | 9353 | Details Get a Quote |
| SLIT2 Knockout A-549 Cell Line | EDJ-KQ63614 | Human | 9353 | Details Get a Quote |
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