Expression of TREM-1 in hepatic stellate cells and prognostic value in hepatitis B-related hepatocellular carcinoma

Cancer Sci. 2012 Jun;103(6):984-92. doi: 10.1111/j.1349-7006.2012.02273.x. Epub 2012 Apr 19.

Abstract

Hepatocellular carcinoma (HCC) is a typical inflammation-related malignancy characterized by high postoperative recurrence and metastasis. Although several inflammatory cells and inflammatory signatures have been linked to poor prognosis, the inflammation-associated molecular mechanisms of HCC development and progression are largely unknown. Here we show that triggering receptor expressed in myeloid cells (TREM)-1, a transmembrane receptor expressing in myeloid cells, was also expressed in tumor-activated hepatic stellate cells (HSCs) and associated with the aggressive behavior of HCC cells. Enzyme-linked immunosorbent assay was used to measure the expression levels of soluble TREM-1 (sTREM-1) in activated hepatic stellate cells supernatant and 92 preoperative and postoperative plasmas of patients with malignancy and/or benign liver tumor/disease, respectively. Expression levels of TREM-1 were assessed by immunohistochemistry in tissue microarray from 240 patients with HCC. As a result, increased secretion of sTREM-1 from activated HSCs was observed after co-culture with HCC cell lines (P < 0.001), and conditioned medium collected from activated HSCs/cancer associated myofibroblasts (CAMFs) with or without agonist/inhibitor of TREM-1 significantly changed the migratory ability of HCC cells. The levels of sTREM-1 were significantly higher in patients with HCC than those with benign liver tumors (P < 0.005). Peritumoral density of TREM-1 was shown to be an independent prognosis predictor according to univariate (P < 0.001 for both overall survival and time to recurrence) and multivariate analysis (P = 0.008 for overall survival; P = 0.005 for time to recurrence). Thus, these observations suggest that TREM-1 is related to the aggressive tumor behavior and has potential value as a prognostic factor for HCC.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma, Hepatocellular / metabolism*
  • Carcinoma, Hepatocellular / mortality
  • Carcinoma, Hepatocellular / pathology
  • Carcinoma, Hepatocellular / virology
  • Cell Movement
  • Cells, Cultured
  • Coculture Techniques
  • Culture Media, Conditioned / chemistry
  • Female
  • Hepatic Stellate Cells / metabolism*
  • Hepatitis B / complications*
  • Hepatitis B virus
  • Hepatocytes / metabolism
  • Humans
  • Inflammation
  • Interleukin-6 / biosynthesis
  • Kaplan-Meier Estimate
  • Liver Neoplasms / metabolism*
  • Liver Neoplasms / mortality
  • Liver Neoplasms / pathology
  • Liver Neoplasms / virology
  • Male
  • Membrane Glycoproteins / agonists
  • Membrane Glycoproteins / antagonists & inhibitors
  • Membrane Glycoproteins / biosynthesis*
  • Middle Aged
  • Myeloid Cells / immunology
  • Myeloid Cells / metabolism
  • Myofibroblasts / metabolism
  • Prognosis
  • Receptors, Immunologic / agonists
  • Receptors, Immunologic / antagonists & inhibitors
  • Receptors, Immunologic / biosynthesis*
  • Triggering Receptor Expressed on Myeloid Cells-1
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Culture Media, Conditioned
  • Interleukin-6
  • Membrane Glycoproteins
  • Receptors, Immunologic
  • TREM1 protein, human
  • Triggering Receptor Expressed on Myeloid Cells-1
  • Tumor Necrosis Factor-alpha