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Neuropeptide Levels as well as Neprilysin Activity Decrease in Renal Cell Carcinoma.
Nuray Erin1, Tümay İpekçi2, Bahar Akkaya3
1Department of Medical Pharmacology, School of Medicine, Akdeniz University, Antalya, Turkey. nerin@akdeniz.edu.tr.
Summary
Neprilysin (NEP) activity and levels are reduced in renal cell carcinoma (RCC), impacting sensory neuropeptides like Calcitonin Gene-related Peptide (CGRP) and Vasoactive Intestinal Peptide (VIP). This loss of NEP activity may hinder VIP
Area of Science:
- Neuropeptide signaling in oncology
- Renal cell carcinoma pathogenesis
- Neuroimmune modulation in cancer
Background:
- Sensory neuropeptides (CGRP, VIP, SP) influence cancer growth via chronic inflammation.
- Neprilysin (NEP) hydrolyzes these neuropeptides; its decreased activity is noted in certain RCC subtypes.
- Altered peptidergic nerve endings and neuropeptide levels in RCC remain largely uncharacterized.
Purpose of the Study:
- To evaluate neuropeptide (CGRP, VIP, SP) levels and NEP activity in renal cell carcinoma (RCC) and adjacent kidney tissue.
- To investigate subtype-specific alterations in neuropeptide and NEP expression within the tumor microenvironment.
- To explore the potential impact of altered neuropeptide metabolism on RCC progression.
Main Methods:
- Cross-sectional study of 57 RCC patients undergoing nephrectomy.
- Measurement of NEP activity, levels (Western blot, qPCR), and expression (immunohistochemistry).
- Quantification of neuronal and non-neuronal CGRP, SP, and VIP using acid extraction techniques.
Main Results:
- NEP activity and levels were significantly decreased in RCC tissues across all subtypes.
- VIP and CGRP levels were elevated in RCC compared to adjacent kidney tissue, with subtype-specific variations.
- Neighboring kidney tissue in papillary RCC showed lower VIP levels than clear cell RCC, indicating differential microenvironment alterations.
Conclusions:
- Renal cell carcinoma (RCC) exhibits reduced Neprilysin (NEP) activity and altered neuropeptide profiles (VIP, CGRP).
- Subtype-specific changes in neuropeptide levels within the tumor microenvironment suggest distinct pathogenetic mechanisms.
- The loss of NEP activity may impair the anti-tumoral effects of Vasoactive Intestinal Peptide (VIP) in RCC, potentially promoting tumor growth.
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