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Updated: Jul 29, 2026
Quantitative Mass Spectrometric Profiling of Cancer-cell Proteomes Derived From Liquid and Solid Tumors
Published on: February 27, 2015
Decoding bladder cancer aggressiveness: A proteomic, phosphoproteomic and metabolomic approach
Zhihui Feng1, Biao Zhang1, Yi Liu1
1Laboratory Central, Guangxi Key Laboratory of Metabolic Reprogramming and Intelligent Medical Engineering for Chronic Diseases, Guangxi Health Commission Key Laboratory of Glucose and Lipid Metabolism Disorders, The Second Affiliated Hospital of Guilin Medical University, Guilin 541199, China.
Background:
Bladder cancer (BC) is the most common malignancy of the urinary system. However, the median survival of patients with metastatic bladder cancer remains limited. Thus, there is an urgent imperative to develop novel biomarkers for BC-targeted therapies and to conduct in-depth investigations into BC pathogenesis leveraging multi-omics technologies.
Results:
Our results revealed that proteins co-upregulated in both proteomic and phosphoproteomic analysis, such as SLC4A7 and MYO9B, demonstrated potential utility in distinguishing MIBC from NMIBC. Upregulation of CPT2 and palmitic acid in MIBC patients highlighted the dysregulation of physiological control mechanisms and enhanced pro-tumorigenic effects of lipid metabolic pathways.
Conclusions:
Integrated multi-omics analysis reveals that key regulatory proteins such as SLC4A7 and MYO9B play pivotal roles in mediating the aggressive phenotypes of MIBC. Aberrant upregulation of CPT2 protein and metabolites like palmitic acid may drive malignant transformation from NMIBC to MIBC by promoting lipid metabolic reprogramming.
Significance:
This study utilized LC-MS/MS to systematically profile the proteomic, phosphoproteomic, and metabolomic characteristics of MIBC, NMIBC, and adjacent noncancerous tissues, with the aim of identifying key molecules and metabolites driving bladder cancer progression. Our findings indicate that aberrant phosphorylation of regulatory proteins such as SLC4A7 and MYO9B may play a critical role in mediating the invasive phenotype of MIBC. In parallel, the upregulation of CPT2 and its associated metabolites (e.g., palmitic acid) suggests that lipid metabolic reprogramming, including enhanced β-oxidation and membrane phospholipid synthesis, may contribute to the malignant transition from NMIBC to MIBC. Overall, this study not only reveals potential molecules and metabolites driving bladder cancer progression but also provides a valuable reference for further exploration of pathways associated with bladder cancer invasiveness.
