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Updated: May 28, 2026

Molecular Profiling of the Invasive Tumor Microenvironment in a 3-Dimensional Model of Colorectal Cancer Cells and Ex vivo Fibroblasts
Published on: April 29, 2014
NIRF is frequently upregulated in colorectal cancer and its oncogenicity can be suppressed by let-7a microRNA
Feng Wang1, Peng Zhang, Yanlei Ma
1Department of Surgery, Sixth People's Hospital Affiliated with Shanghai Jiao Tong University, Shanghai, China.
Abstract:
Np95 ICBP90 RING finger (NIRF) is essential for the regulation of cell proliferation and has been implicated in tumorigenesis. However, the role of NIRF in colorectal cancer (CRC) remains unclear. In this study, we demonstrated that NIRF expression was aberrantly increased in CRC tissues and associated with poor overall survival. Bioinformatics analysis indicated that NIRF was a putative target of the microRNA let-7a, which was confirmed by luciferase reporter assay. We then demonstrated in vitro that enforced expression of let-7a, or knockdown of NIRF, led to reduced CRC cell proliferation due to cell cycle arrest at the G0/G1 phase and reduced cell migration. Finally, an in vivo tumorigenicity assay in nude mice showed that synthetic let-7a suppressed NIRF expression and reduced tumor growth. Taken together, our results provide new evidence that NIRF has an oncogenic role in CRC. This opens up the possibility of targeting NIRF and let-7a for CRC therapy.
Insights
Np95 ICBP90 RING finger (NIRF) is overexpressed in colorectal cancer (CRC), promoting tumor growth and poor survival. Targeting NIRF with microRNA let-7a offers a potential therapeutic strategy for CRC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Np95 ICBP90 RING finger (NIRF) is crucial for cell proliferation and tumorigenesis.
- The specific role of NIRF in colorectal cancer (CRC) pathogenesis is not well understood.
Purpose of the Study:
- To investigate the role of NIRF in colorectal cancer (CRC).
- To explore the regulatory relationship between NIRF and microRNA let-7a in CRC.
Main Methods:
- Quantitative analysis of NIRF expression in CRC tissues.
- Bioinformatics analysis and luciferase reporter assays to confirm let-7a targeting of NIRF.
- In vitro cell proliferation, cell cycle, and migration assays.
- In vivo tumorigenicity assays in nude mice.
Main Results:
- NIRF expression is significantly elevated in CRC tissues and correlates with poorer patient survival.
- let-7a directly targets and downregulates NIRF expression.
- Overexpression of let-7a or knockdown of NIRF inhibits CRC cell proliferation, induces G0/G1 cell cycle arrest, and reduces cell migration.
- Therapeutic administration of let-7a suppressed tumor growth in vivo by reducing NIRF expression.
Conclusions:
- NIRF plays an oncogenic role in colorectal cancer (CRC).
- The NIRF-let-7a axis represents a potential therapeutic target for CRC treatment.
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