Pancreatic cancer-derived S-100A8 N-terminal peptide: A diabetes cause?

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• 作者：Daniela Basso ; Eliana Greco ; Paola Fogar ; Piero Pucci ; Angela Flagiello ; Goretta Baldo ; Silvia Giunco ; Anna Valerio ; Filippo Navaglia ; Carlo-Federico Zambon et al.
• 刊名：Clinica Chimica Acta
• 出版年：2006
• 出版时间：October 2006
• 年：2006
• 卷：372
• 期：1-2
• 页码：120-128
• 全文大小：332 K

文摘

Background

Our aim was to identify the pancreatic cancer diabetogenic peptide.

Methods

Pancreatic tumor samples from patients with (n = 15) or without (n = 7) diabetes were compared with 6 non-neoplastic pancreas samples using SDS-PAGE.

Results

A band measuring approximately 1500 Da was detected in tumors from diabetics, but not in neoplastic samples from non-diabetics or samples from non-neoplastic subjects. Sequence analysis revealed a 14 amino acid peptide (1589.88 Da), corresponding to the N-terminal of the S100A8. At 50 nmol/L and 2 mmol/L, this peptide significantly reduced glucose consumption and lactate production by cultured C₂C₁₂ myoblasts. The 14 amino acid peptide caused a lack of myotubular differentiation, the presence of polynucleated cells and caspase-3 activation.

Conclusions

The 14 amino acid peptide from S100A8 impairs the catabolism of glucose by myoblasts in vitro and may cause hyperglycemia in vivo. Its identification in biological fluids might be helpful in diagnosing pancreatic cancer in patients with recent onset diabetes mellitus.