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Updated: Sep 11, 2025

From a 2DE-Gel Spot to Protein Function: Lesson Learned From HS1 in Chronic Lymphocytic Leukemia
Published on: October 19, 2014
FEN1 plays a key role in the transition from HSIL to CSCC
Fengxian Zhang1, Xiaomei Chen1, Chenyang Chu1
1School of Traditional Chinese Medicine, Southern Medical University, Baiyun District, Guangzhou, 510515, China.
High-grade squamous intraepithelial lesion (HSIL) can progress to cervical squamous cell carcinoma (CSCC). This study identifies FEN1 as a key gene overexpressed in both HSIL and CSCC, suggesting it as a therapeutic target to halt cancer progression.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- Cervical high-grade squamous intraepithelial lesion (HSIL) is a recognized precursor to cervical squamous cell carcinoma (CSCC).
- Understanding the molecular mechanisms driving this transition is crucial for early intervention and treatment.
Purpose of the Study:
- To explore molecular mechanisms underlying the transition from HSIL to CSCC.
- To identify potential biomarkers and therapeutic targets for early-stage cervical cancer.
Main Methods:
- Utilized gene expression data from HSIL and CSCC datasets.
- Employed Weighted Gene Coexpression Network Analysis (WGCNA), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) for enrichment analysis.
- Analyzed the tumor immune microenvironment (TIME) using CIBERSORT, performed survival analysis, and investigated FEN1-PCNA interactions.
Main Results:
- Identified 30 shared genes as potential drug targets.
- FEN1 was significantly overexpressed in HSIL and CSCC, correlating with poorer prognosis.
- FEN1 interacts with PCNA, influencing macrophage-mediated immune infiltration and immune escape.
Conclusions:
- FEN1 is a key driver in cervical cancer progression from HSIL to CSCC.
- FEN1 represents a promising biomarker and therapeutic target for preventing or reversing CSCC development.
- Targeting FEN1 with small molecule inhibitors may offer a novel treatment strategy.
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