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5-Aminoisoquinolinone reduces the expression of vascular endothelial growth factor-C via the nuclear factor-κB
Wei-Qiang Wu1, Nilufer Jasmine Selimah Fauzee, Ya-Lan Wang
1Department of Pathology, Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, China.
Objective:
VEGF-C has recently been identified as a key molecule which is involved in tumor lymphangiogenesis. The aim of this research was to investigate the role of PARP-1 inhibition in the regulation of VEGF-C expression in CT26 cells.
Methods:
CT26 cells were treated with or without the PARP-1 inhibitor 5-aminoisoquinolinone (5-AIQ). The expression of PARP-1, NF-kB, and VEGF-C proteins in CT26 cells was measured by Western blot analysis and the VEGF-C mRNA level was determined by reverse transcription polymerase chain reaction (RT-PCR). CT26-secreted VEGF-C was detected by enzyme-linked immunosorbent assay (ELISA).
Results:
The results of Western blot analysis showed that the expression levels of PARP-1, NF-kB, and VEGF-C were reduced in 5-AIQ treated CT26 cells and the levels of VEGF-C mRNA in 5-AIQ treated CT26 were significantly lower than t in 5-AIQ-untreated cells (P<0.05). The concentrations of CT26-secreted VEGF-C were also dramatically decreased (P<0.05).
Conclusion:
Here, we provide evidence for the first time that PARP-1 inhibition dramatically reduces VEGF-C expression via the nuclear factor NF-kB signaling pathway. We therefore propose that PARP-1 inhibition has an anti-lymphangiogenic effect and may contribute to the prevention of metastatic dissemination via the lymphatic system.
Insights
PARP-1 inhibition significantly reduces VEGF-C expression and its mRNA levels in CT26 cells, suggesting an anti-lymphangiogenic effect. This finding highlights PARP-1 inhibition as a potential strategy against tumor metastasis.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Vascular Endothelial Growth Factor C (VEGF-C) is crucial for tumor lymphangiogenesis.
- Understanding the regulation of VEGF-C is vital for developing anti-metastatic therapies.
Purpose of the Study:
- To investigate the effect of Poly(ADP-ribose) polymerase-1 (PARP-1) inhibition on VEGF-C expression in CT26 cells.
- To elucidate the role of PARP-1 in the regulation of VEGF-C via the NF-kB signaling pathway.
Main Methods:
- CT26 cells were treated with the PARP-1 inhibitor 5-aminoisoquinolinone (5-AIQ).
- Protein expression of PARP-1, NF-kB, and VEGF-C was analyzed using Western blot.
- VEGF-C mRNA levels were quantified via RT-PCR.
- Secreted VEGF-C was measured by ELISA.
Main Results:
- PARP-1 inhibition with 5-AIQ reduced protein expression of PARP-1, NF-kB, and VEGF-C in CT26 cells.
- VEGF-C mRNA levels were significantly decreased in 5-AIQ treated cells compared to controls (P<0.05).
- Concentrations of secreted VEGF-C were dramatically reduced by 5-AIQ treatment (P<0.05).
Conclusions:
- PARP-1 inhibition effectively reduces VEGF-C expression through the NF-kB signaling pathway.
- PARP-1 inhibition demonstrates an anti-lymphangiogenic effect in CT26 cells.
- Targeting PARP-1 may represent a novel therapeutic strategy to prevent lymphatic metastasis.
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