Expression of gap junction protein connexin 26 in human hepatocellular carcinoma and its significance / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the expression of gap junction protein connexin 26(Cx26) in hepatocellular carcinoma(HCC) and its significance.</p><p><b>METHODS</b>The expression of Cx26 in liver tissue was examined by immunohistochemistry staining in 159 paraffin-embeded liver sections, including 20 samples of normal liver tissue, 30 samples of chronic hepatitis, 33 samples of liver cirrhosis, and 76 samples of HCC. Normal hepatic cell line LO2 and HCC cell line SMMC-7721 were used in vitro to verify the characteristics of gap junction and Cx26 expression pattern. The expression and localization of Cx26 were measured by Western blotting and immunofluorescence assay, respectively. The function of gap junction between adjacent cells was detected by dye transfer assay.</p><p><b>RESULTS</b>Compared to normal liver samples, the positive rate of Cx26 was markedly decreased in hepatitis, cirrhosis and HCC tissues(all P<0.05). The intensity of Cx26 staining was significantly increased in HCC tissues compared with those in non-carcinomatous liver(NCL) tissues(all P<0.05). In NCL tissues, there was a mild to moderated staining of Cx26 which located mainly on the membranes of hepatocytes at intercellular contacts. The positive staining of Cx26 in HCC tissues was observed mainly in cytoplasm. Positive Cx26 expression was positively associated with tumor size(P=0.036), but not with age, gender, histologic grade, clinical stage, underlying hepatitis and cirhosis, lymph node metastasis and intrahepatic vascular embolism(all P>0.05). Compared with LO2 cells, an aberrant expression and distribution of Cx26 in SMMC-7721 cells was confirmed, which may lead to a decreased function of gap junctions.</p><p><b>CONCLUSIONS</b>The aberrant expression and distribution of Cx26 protein may be associated with hepatocarcinogenesis, and the residual gap junction in HCC may provide a new target for treatment of HCC.</p>

Expression of secreted frizzled related protein 1, β-catenin and E-cadherin in colorectal carcinoma and its clinicopathological significances / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the expression of secreted frizzled-related protein 1 (SFRP1), β-catenin and E-cadherin in colorectal carcinoma and its clinicopathological significance.</p><p><b>METHODS</b>The expression of SFRP1, β-catenin and E-cadherin mRNA and protein in tumor and pericancerous tissue samples from 60 cases of colorectal cancer was assayed by reverse-transcription PCR and immunohistochemistry, respectively. The correlation of their expression with clinicopathological factors of colorectal cancer was analyzed.</p><p><b>RESULTS</b>In 52/60 cases the relative mRNA expression of SFRP1 in cancer tissue and pericancerous tissue was 0.4837±0.1532 and 0.7170 ±0.1830; for β-catenin was 0.9293± 0.3705 and 0.6469±0.3166; and for E-cadherin was 0.5556±0.2535 and 0.9422±0.2372 (P<0.01), respectively. SFRP1 mRNA expression was associated with lymphatic metastasis (P<0.05). The positive rate of SFRP1 in colorectal cancer was 31.67% (19/60), and was significantly lower than that in pericancerous colorectal mucosa (75.00%, 45/60). No relationship between SFRP1 protein expression and clinical pathology was found. Abnormal expression rates of β-catenin and E-cadherin in colorectal cancer were 75.00% (45/60) and 58.33% (35/60), respectively, which were significantly higher than that in pericancerous colorectal mucosa (1.67% and 6.67%), respectively. Abnormal β-catenin and E-cadherin expression was associated with tumor differentiation, lymphatic metastasis and Duke's staging. SFRP1 protein expression was negatively correlated with β-catenin and E-cadherin expression (r=-0.517, -0.442, Ps<0.01).</p><p><b>CONCLUSION</b>Down-regulation of SFRP1 in colorectal cancer may cause abnormal Wnt signaling and induce abnormal β-catenin and E-cadherin expression, indicating that SFRP1 might be involved in the development and progression of colorectal cancer, and could be a novel therapeutic target for colorectal cancer.</p>