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A multifactorial analysis of FAP to regulate gastrointestinal cancers progression
Jialing Cai1, Depeng Yang1, Handi Sun1
1School of Life Science and Technology, Harbin Institute of Technology, Harbin, Heilongjiang, China.
Frontiers in Immunology
|June 16, 2023
Summary
Fibroblast activation protein (FAP) is upregulated in gastrointestinal cancers, promoting tumor cell movement and M2 macrophage polarization. This study reveals FAP
Area of Science:
- Oncology
- Cancer Biology
- Immunology
Background:
- Fibroblast activation protein (FAP) is a serine protease upregulated in fibrotic and cancerous tissues.
- FAP's role in gastrointestinal (GI) cancers is not fully understood, despite its known importance in cancer progression.
- Limited multifactorial analyses exist for FAP's function in GI malignancies.
Purpose of the Study:
- To comprehensively evaluate the carcinogenesis potential of FAP in GI cancers.
- To analyze the correlation between FAP expression and patient outcomes, and tumor immunology.
- To experimentally validate FAP's pro-tumor and immune-regulatory roles in GI cancers, using liver cancer as a model.
Main Methods:
- Utilized datasets from TCGA, CPTAC, scTIME Portal, and HPA for bioinformatic analysis.
- Investigated FAP expression and correlation with outcomes and immune infiltration in liver, colon, pancreas, and stomach cancers.
- Performed in vitro experiments overexpressing FAP in LX2 cells to assess effects on GI cancer cells and macrophages.
Main Results:
- FAP is abundantly expressed in LIHC, COAD, PAAD, and STAD, correlating with extracellular matrix organization.
- High FAP expression is linked to increased M2 macrophage infiltration across these GI cancers.
- Overexpressing FAP in LX2 cells promoted GI cancer cell motility and M2 macrophage polarization and invasion.
Conclusions:
- FAP is significantly upregulated in fibroblasts within GI cancers.
- FAP contributes to tumor cell motility, macrophage infiltration, and M2 polarization.
- This study highlights the multifactorial role of FAP in driving GI cancer progression.
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