1. Overexpression of the key metabolic protein Carnitine Palmitoyl Transferase 1A (CPT1A) in equine sarcoid.
- Author
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Martano M, Power K, Cuccaro B, Razzuoli E, Maiolino P, and Restucci B
- Subjects
- Animals, Horses, Skin Neoplasms veterinary, Skin Neoplasms pathology, Skin Neoplasms metabolism, Skin Neoplasms enzymology, Gene Expression Regulation, Neoplastic, Gene Expression Regulation, Enzymologic, Sarcoidosis pathology, Sarcoidosis metabolism, Sarcoidosis veterinary, Sarcoidosis enzymology, Fibroblasts metabolism, Fibroblasts pathology, Carnitine O-Palmitoyltransferase metabolism, Carnitine O-Palmitoyltransferase genetics, Horse Diseases metabolism, Horse Diseases pathology, Horse Diseases enzymology
- Abstract
The equine sarcoid is the most common skin neoplasia of fibroblastic origin in horses, characterized by an excessive accumulation of extracellular matrix produced by sarcoid fibroblasts under hypoxic condition. Neoplastic cells can adapt to hypoxia by using alternative energy sources, particularly those that arise from fatty acid oxidation (FAO). The Carnitine Palmitoyl Transferase 1A (CPT1A) belongs to Carnitine System (CS) and promotes the entrance of fatty acids into the mitochondria for β-oxidation. In this study, CPT1A expression was comparatively addressed in 25 equine sarcoids and 5 normal skin samples using immunohistochemistry (IHC). Specificity of CPT1A antibody was validated by Western Blotting (WB). In normal skin samples IHC staining was weak and mainly confined to basal epidermis and few dermal fibroblasts. Sarcoid fibroblast exhibited a strong cytoplasmic and nuclear signal in 60% of the tumor samples. Cytoplasmic CPT1A expression in sarcoid fibroblasts indicates that the protein is actively involved in metabolic reprogramming processes. Nuclear CPT1A expression suggests that the protein may also be involved in the regulation of neoplastic proliferation., Competing Interests: Declaration of competing interest None of the authors has any financial or personal relationships that could inappropriately influence or bias the content of the paper, (Copyright © 2024. Published by Elsevier Inc.)
- Published
- 2024
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