Journal of Southern Medical University ›› 2015, Vol. 35 ›› Issue (12): 1705-.

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Correlation of triggering receptors expressed on myeloid cells-1 with the oncogenesis and
progression of hepatocellular carcinoma

  

  • Online:2015-12-20 Published:2015-12-20

Abstract: Objective To investigate the role of triggering receptors expressed on myeloid cells-1 (TREM-1) in the oncogenesis
and progression of hepatocellular carcinoma (HCC). Methods The expression and localization of TREM-1 were detected by
immunohistochemistry in 76 specimens of HCC, 33 specimens of liver cirrhosis, 30 specimens of hepatitis and 20 normal liver
tissues. The association between TREM-1 expression and the clinicopathologic parameters of HCC was analyzed. Human
normal hepatic cell line LO2 and HCC cell line SMMC-7721 were examined for TREM-1 expression pattern using RT-PCR and
Western blotting. Results All the normal liver samples showed negative expression of TREM-1 protein, which was significantly
up-regulated in the other 3 tissues. The positivity rates of TREM-1 expression were not significantly different between
hepatitis, cirrhosis and HCC tissues [20.00% (6/30), 24.24% (8/33), and 21.05% (16/76), respectively; χ2=0.195, P=0.907]. Different
from chronic hepatitis and liver cirrhosis tissues where TREM-1 expression was located mainly in the nucleus and occasionally
in the cytoplasm of the hepatocytes, HCC tissues showed a cellular localization of TREM-1 protein almost exclusively in the
cytoplasm. In HCC, TREM-1 expression was negatively correlated with the histological grade of the tumor (r=-0.261, P=0.023)
but not related with the patients’ age, gender, tumor size, clinical stage, pre-existing hepatitis and cirrhosis, lymph node
metastasis, or intrahepatic vascular embolism (all P>0.05). In the in vitro experiments, low levels of TREM-1 mRNA and protein
expressions were detected in LO2 cells line, but their expressions were markedly up-regulated in SMMC-7721 cells.
Conclusion Aberrant enhancement of the expression and cytoplasmic accumulation of TREM-1 may correlate closely with the
oncogenesis and progression of HCC.