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Itraconazole can inhibit malignant pleural effusion by suppressing lymphangiogenesis in mice
Yunfen Wang1, Yanwen Yao1, Hongbin Liu1
11 Department of Respiratory Medicine, Jinling Hospital, Nanjing Clinical School of Southern Medical University, Nanjing 210002, China ; 2 Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing 210002, China ; 3 Department of Medical Oncology, 81 Hospital of PLA, Nanjing 210002, China.
Background:
The presence of malignant pleural effusion (MPE) indicates a poor prognosis in patients with non-small cell lung cancer (NSCLC). Itraconazole has been identified as a potent inhibitor of endothelial cell proliferation that suppresses angiogenesis; however, its role in the suppression of lymphangiogenesis is still unclear. The aim of this study was to investigate the efficacy of itraconazole for MPE and the mechanism of lymphangiogenesis suppression.
Methods:
Lewis lung carcinoma (LLC) cells were injected into the mouse pleural cavity to establish the MPE mouse model, followed by randomization of the mice into three groups. Each mice was injected with either a high dose of itraconazole (25 mg/kg, H-ITCZ), a low dose of itraconazole (8 mg/kg, L-ITCZ), or 50 μL of hydroxypropyl-β-cyclodextrin (130 mg/mL, H-β-C) into the pleural cavity four times every 3 days. The MPE of the mice was collected and measured with a 1 mL syringe. The vascular endothelial growth factor-C (VEGF-C) expression level in the MPE was detected by enzyme-linked immunosorbent assay (ELISA), while the VEGF-C expression and lymphatic micro vessel density (LMVD) in the tumor tissue was observed by immunohistochemistry (IHC) staining.
Results:
The number of pleural tumor foci, the volume of pleural effusion, the LMVD and the VEGF-C expression levels in the tumor tissue were significantly reduced in the H-ITCZ-treated group.
Conclusions:
Our results revealed that itraconazole may play an important role in the MPE mice by suppressing lymphangiogenesis, which demonstrated the usefulness of itraconazole in the treatment of MPE.
Insights
Itraconazole significantly reduced pleural effusion and tumor growth in mice with malignant pleural effusion (MPE) by suppressing lymphangiogenesis. This study highlights itraconazole
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Malignant pleural effusion (MPE) is a poor prognostic indicator in non-small cell lung cancer (NSCLC).
- Itraconazole inhibits endothelial cell proliferation and angiogenesis, but its effect on lymphangiogenesis is not well understood.
Purpose of the Study:
- To investigate the efficacy of itraconazole in treating MPE.
- To elucidate the mechanism by which itraconazole suppresses lymphangiogenesis in MPE.
Main Methods:
- A mouse model of MPE was established using Lewis lung carcinoma (LLC) cells.
- Mice received high-dose itraconazole (H-ITCZ), low-dose itraconazole (L-ITCZ), or a control vehicle.
- Pleural effusion volume, tumor foci, vascular endothelial growth factor-C (VEGF-C) levels, and lymphatic microvessel density (LMVD) were assessed.
Main Results:
- High-dose itraconazole significantly reduced pleural tumor foci and effusion volume.
- H-ITCZ treatment led to a significant decrease in LMVD and VEGF-C expression in tumor tissues.
Conclusions:
- Itraconazole demonstrates efficacy in treating MPE in a mouse model.
- The mechanism involves the suppression of lymphangiogenesis, indicated by reduced LMVD and VEGF-C.
- These findings suggest itraconazole's potential as a therapeutic agent for MPE.
