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Updated: Jan 22, 2026

Orthotopic Mouse Model of Colorectal Cancer
Published on: December 4, 2007
FPR2 enhances colorectal cancer progression by promoting EMT process
1Department of General Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
Formyl peptide receptor-2 (FPR2) promotes colorectal cancer (CRC) progression by enhancing cell proliferation, migration, invasion, and angiogenesis. Silencing FPR2 suppressed tumor growth and may involve regulating epithelial-mesenchymal transition (EMT).
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Formyl peptide receptor-2 (FPR2) is implicated in various cancers.
- The specific role of FPR2 in colorectal cancer (CRC) requires further elucidation.
Purpose of the Study:
- To investigate the impact of FPR2 interference on CRC cell proliferation, migration, invasion, apoptosis, and angiogenesis.
- To explore the underlying mechanisms, including epithelial-mesenchymal transition (EMT).
Main Methods:
- Quantitative PCR to assess FPR2 expression in CRC tissues.
- FPR2 gene knockdown in SW1116 CRC cell line using sh-RNA.
- In vitro assays for proliferation, migration, invasion, apoptosis, and angiogenesis; in vivo tumorigenesis in nude mice; Western blotting for EMT markers.
Main Results:
- FPR2 mRNA was highly expressed in colorectal cancer tissues.
- Silencing FPR2 significantly suppressed CRC cell proliferation, migration, invasion, and pro-angiogenesis, while promoting apoptosis.
- FPR2 knockdown inhibited tumor growth in vivo and altered the expression of EMT-related proteins.
Conclusions:
- FPR2 promotes colorectal cancer progression both in vitro and in vivo.
- The pro-tumorigenic effects of FPR2 in CRC may be mediated through the regulation of epithelial-mesenchymal transition (EMT).
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