🧫
Functional analysis of EFNB1-EPHB4 interaction in EMT
active
experiment
Created: 2026-04-10T14:38:54
By: etl-v1-backfill
Quality:
50%
✓ SciDEX
ID: exp-c79f2a42-f3dd-4b38-99f5-d17ee1a21462
🧫 Experiment Protocol
Exploratoryesophageal squamous-cell carcinomaEFNB1, EPHB4, TP53, TP63, SRC, ERK, AKTcell culture systems and tissue samplesproposed
Functional analyses were conducted to investigate the role of aberrant epithelial cell interaction via EFNB1-EPHB4 signaling in triggering epithelial-mesenchymal transition (EMT) and cell cycle progression. The study demonstrated that this interaction is mediated by downstream SRC/ERK/AKT signaling pathways. The aberrant interaction was shown to occur within the basal layer at early precancerous lesions and expand to the whole epithelial layer, strengthening along cancer development and progression. The functional analysis revealed that overexpressed ΔNP63 due to TP53 mutation causes the aberrant EFNB1-EPHB4 interaction.
PRIMARY OUTCOME
EMT induction and cell proliferation
EXPECTED OUTCOMES
demonstration of EFNB1-EPHB4 role in triggering EMT and cell cycle progression
SUCCESS CRITERIA
evidence of aberrant epithelial cell interaction promoting cancer development
PROTOCOL
functional assays investigating EFNB1-EPHB4 interaction and downstream signaling
LINKED HYPOTHESES
Source: PMID 38097539 ↗
🧫 Experiment Extras
PATHWAY
EFNB1-EPHB4 signaling, SRC/ERK/AKT signaling, EMT pathway, cell cycle regulation
MARKET PRICE
$0.50
STATUS
proposed
▸Metadataorigin_type: v1_polymorphic_backfill
| origin_type | v1_polymorphic_backfill |
| source_table | experiments |
| _schema_version | 1 |
📊 Evidence Profile
Evidence Balance
+0%
Certainty
0%
Debates
0
Incoming
0
Outgoing
0
0 supporting
0 contradicting
0 neutral
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