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Anti-chloride Intracellular Channel Protein 1 (CLIC1) Antibodies Induce Tumour Necrosis and Angiogenesis Inhibition
Andrei Dan Radu-Cosnita1, Alexandru Nesiu2, Patricia Lorena Berzava3,4
1Department IX, Surgery I/Ophthalmology, Victor Babes University of Medicine and Pharmacy, Timisoara, Romania.
Background/Aim:
Chloride intracellular channel protein 1 (CLIC1) is known as a promoter of cancer progression, metastasis, and angiogenesis. Thus, CLIC1 could be a future therapeutic target. This study aimed to evaluate the effect of anti-CLIC1 antibodies on tumour cells and vessels of human renal cell carcinoma (RCC) in rabbit cornea and chick embryo chorioallantoic membrane (CAM) models.
Materials And Methods:
Human cc-RCC xenografts on rabbit cornea and CAM surface were performed. Anti-CLIC1 antibodies were applied for 5 consecutive days on both tumor models. We comparatively evaluated treated and untreated tumors by combining ultrasonography with microscopic techniques.
Results:
RCC implants rapidly recruited blood vessels and had an exponential growth rate on both tumor models. Anti-CLIC1 antibodies suppressed tumor growth by inducing tumor cell necrosis. Tumor vessels regressed rapidly but not completely during anti-CLIC1 antibodies based therapy.
Conclusion:
Anti-CLIC1 antibodies induced tumor necrosis and tumor vasculature regression in human cc-RCC xenografts in both in vivo experimental models.
Insights
Anti-CLIC1 antibodies effectively reduced renal cell carcinoma (RCC) growth by causing tumor cell death and decreasing tumor blood vessel formation in preclinical models.
Area of Science:
- Oncology
- Immunology
- Vascular Biology
Background:
- Chloride intracellular channel protein 1 (CLIC1) promotes cancer progression, metastasis, and angiogenesis.
- CLIC1 represents a potential therapeutic target for cancer treatment.
Purpose of the Study:
- To investigate the therapeutic potential of anti-CLIC1 antibodies against human renal cell carcinoma (RCC).
- To evaluate the effects of anti-CLIC1 antibodies on tumor cells and vasculature in vivo.
Main Methods:
- Human cc-RCC xenografts were established in rabbit cornea and chick embryo chorioallantoic membrane (CAM) models.
- Anti-CLIC1 antibodies were administered for five consecutive days.
- Tumor growth and vascularization were assessed using ultrasonography and microscopy.
Main Results:
- RCC xenografts exhibited rapid vascular recruitment and exponential growth.
- Anti-CLIC1 antibody treatment suppressed tumor growth through induced tumor cell necrosis.
- Therapy with anti-CLIC1 antibodies led to rapid, though incomplete, regression of tumor vasculature.
Conclusions:
- Anti-CLIC1 antibodies demonstrated efficacy in inducing tumor cell necrosis.
- Treatment with anti-CLIC1 antibodies resulted in significant tumor vasculature regression in human cc-RCC xenografts.
- These findings support CLIC1 as a viable therapeutic target for renal cell carcinoma.
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