Macrophage inflammatory protein-3alpha is a novel serum marker for nasopharyngeal carcinoma detection and prediction of treatment outcomes

Clin Cancer Res. 2008 Nov 1;14(21):6979-87. doi: 10.1158/1078-0432.CCR-08-0090.

Abstract

Purpose: We herein examine whether macrophage inflammatory protein-3alpha (MIP-3alpha) is a biomarker for nasopharyngeal carcinoma (NPC) and whether it is involved in modulating NPC cell functions.

Experimental design: The study population comprises 275 NPC patients and 250 controls. MIP-3alpha levels in tissues and sera were examined by immunohistochemistry and ELISA, respectively. EBV DNA load and EBV viral capsid antigen IgA were measured by quantitative real-time PCR and immunofluorescence assay, respectively. Effects of MIP-3alpha on NPC cell motility were investigated by Transwell migration/invasion assays and RNA interference.

Results: MIP-3alpha was overexpressed in NPC tumor cells. Serum MIP-3alpha levels were significantly higher in untreated patients, recurrent patients and patients with distant metastases versus non-NPC controls, patients with complete remission, and long-term disease-free patients. In the prospective cohort, serum MIP-3alpha levels were significantly higher in untreated NPC patients with advanced tumor-node-metastasis stage versus early stage and also correlated with EBV DNA load. Measurement of MIP-3alpha, EBV DNA, and viral capsid antigen IgA levels in serial serum/plasma samples from treated patients at 6-month intervals revealed a high association between MIP-3alpha level, EBV DNA load, and disease status. Among 155 consecutive NPC patients, subjects with pretreated MIP-3alpha serum levels over 65 pg/mL had worse prognoses for overall survival and distant metastasis-free survival in univariate and multivariate analysis. Additionally, cell functional assays showed that MIP-3alpha contributed to migration and invasion of NPC cells, which could be effectively inhibited by MIP-3alpha knockdown.

Conclusions: MIP-3alpha may be a novel biomarker and prognosticator for NPC and is involved in migration and invasion of NPC cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, Viral / analysis
  • Biomarkers, Tumor / analysis*
  • Capsid Proteins / analysis
  • Cell Movement
  • Chemokine CCL20 / blood*
  • DNA, Viral / analysis
  • Disease-Free Survival
  • Female
  • Herpesvirus 4, Human / genetics
  • Humans
  • Male
  • Middle Aged
  • Nasopharyngeal Neoplasms / blood*
  • Nasopharyngeal Neoplasms / diagnosis
  • Neoplasm Metastasis
  • Prognosis

Substances

  • Antigens, Viral
  • Biomarkers, Tumor
  • CCL20 protein, human
  • Capsid Proteins
  • Chemokine CCL20
  • DNA, Viral
  • Epstein-Barr viral capsid antigen