EGFR conjunct FSCN1 as a Novel Therapeutic Strategy in Triple-Negative Breast Cancer
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Updated: Feb 18, 2026

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells
Published on: January 18, 2017
Chao-Qun Wang1, Yang Li2, Bi-Fei Huang1
1Department of Pathology, Affiliated Dongyang Hospital of Wenzhou Medical University, Dongyang, 322100, Zhejiang, China.
Abstract:
Emerging evidence indicates that Fascin-1 (FSCN1) may possess a causal role in the development of several types of cancers and serves as a novel biomarker of aggressiveness in certain carcinomas. However, the regulatory mechanism of FSCN1 in triple-negative breast cancer (TNBC) cell invasion and migration is still largely unknown. In our study, we observed that the FSCN1 expression rates were significantly higher in invasive ductal carcinoma, compared with both usual ductal hyperplasia and ductal carcinoma in situ. FSCN1 expression was significantly higher in cases of TNBC compared with the non-TNBC subtype. Overexpression of FSCN1 promoted TNBC cell migration and invasion. Epidermal growth factor induced the expression of FSCN1 through activation of MAPK, which subsequently promoted cell migration and invasion. A significant decrease in FSCN1 expression following the co-treatment of FSCN1 siRNA and Gefitinib, compared with the separate treatment of FSCN1 siRNA or Gefitinib. Furthermore, we found that there was a significant association between FSCN1 expression and poor relapse-free survival and overall survival. Therefore, we suggest that co-targeting epidermal growth factor receptor and FSCN1 dual biomarker may be used as a novel therapeutic strategy for TNBC.
Insights
Fascin-1 (FSCN1) drives triple-negative breast cancer (TNBC) cell invasion and migration. Targeting both FSCN1 and epidermal growth factor receptor offers a new therapeutic strategy for TNBC.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Biomarkers
Background:
- Fascin-1 (FSCN1) is implicated in various cancers and may indicate aggressiveness.
- The regulatory mechanisms of FSCN1 in triple-negative breast cancer (TNBC) cell invasion and migration are not well understood.
Purpose of the Study:
- To investigate the role of FSCN1 in TNBC cell invasion and migration.
- To explore the regulatory pathway of FSCN1 in TNBC.
- To assess the prognostic value of FSCN1 in breast cancer patients.
Main Methods:
- Comparative analysis of FSCN1 expression in different breast cancer subtypes and stages.
- In vitro studies using cell lines to assess the impact of FSCN1 overexpression on migration and invasion.
- Investigating the role of epidermal growth factor (EGF) and MAPK signaling in FSCN1 regulation.
- Evaluating the combined effect of FSCN1 siRNA and Gefitinib on FSCN1 expression.
- Statistical analysis of the association between FSCN1 expression and patient survival outcomes.
Main Results:
- FSCN1 expression is significantly higher in invasive ductal carcinoma than in pre-invasive lesions.
- FSCN1 is significantly upregulated in TNBC compared to non-TNBC subtypes.
- FSCN1 overexpression enhances TNBC cell migration and invasion.
- Epidermal growth factor (EGF) induces FSCN1 expression via MAPK activation, promoting cell motility.
- Combined treatment with FSCN1 siRNA and Gefitinib more effectively reduces FSCN1 expression than monotherapy.
- Elevated FSCN1 expression correlates with poor relapse-free and overall survival.
Conclusions:
- FSCN1 plays a critical role in promoting TNBC cell invasion and migration.
- The EGF/MAPK pathway regulates FSCN1 expression in TNBC.
- FSCN1 is a potential prognostic biomarker for TNBC.
- Co-targeting the epidermal growth factor receptor and FSCN1 presents a promising therapeutic strategy for TNBC.
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