Correlation of triggering receptors expressed on myeloid cells-1 with the oncogenesis and progression of hepatocellular carcinoma / 南方医科大学学报

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the role of triggering receptors expressed on myeloid cells-1 (TREM-1) in the oncogenesis and progression of hepatocellular carcinoma (HCC).</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>Aberrant enhancement of the expression and cytoplasmic accumulation of TREM-1 may correlate closely with the oncogenesis and progression of HCC.</p>