Proteomic and amino acid profiling of SK-MEL-30 melanoma reveals metabolic and structural changes
- Anal Biochem. 2026 Nov:718:116205. doi: 10.1016/j.ab.2026.116205.
- 1. Trakya University Technology Research and Development Centre, Edirne, 22030, Turkey. Electronic address: [email protected].
Melanoma exhibits high metastatic potential and therapy resistance, driven by metabolic flexibility and structural remodeling. In this study, we performed an integrated analysis of the SK-MEL-30 Melanoma cell line using function-focused quantitative proteomics and amino acid profiling. Proteins were quantified using a label-free normalized spectral abundance factor (NSAF) approach, while intracellular Amino acids were measured by LC-MS/MS. Functional enrichment analyses based on KEGG and Gene Ontology were used to associate protein expression patterns with metabolic pathways. A total of 148 proteins were identified, predominantly representing high-abundance and functionally relevant components of metabolic and structural pathways. Key cytoskeletal proteins, including vimentin and S100A11, were among the most abundant, consistent with a mesenchymal-like and potentially invasive phenotype. Metabolic profiling revealed elevated expression of glycolytic Enzymes such as PKM and LDHA, consistent with a glycolytic shift. Increased levels of l-glutamine and l-glutamic acid, together with GOT2 expression, suggest an active glutamine aspartate axis supporting Tricarboxylic Acid Cycle activity and nitrogen metabolism. In addition, elevated levels of stress-response proteins, including HSP90 and SOD2, indicate a proteostatic network adapted to metabolic stress. Although the proteome coverage is lower than that reported in large-scale deep proteomic studies, the NSAF-based workflow was designed to capture the most abundant and functionally relevant proteins, providing a focused overview of the major metabolic and structural characteristics of SK-MEL-30 Melanoma cells. Overall, this integrative analysis highlights the coordination between metabolic reprogramming and cytoskeletal organization in SK-MEL-30 cells and suggests that glutamine-dependent metabolic pathways warrant further investigation as potential therapeutic targets in Melanoma.