B Sun1, J Zhang, B Wang. 1. Department of Clinical Immunology, Tongji Hospital of Tongji Medical University, Wuhan 430030, China.
Abstract
OBJECTIVE: To investigate the relationship between caspase3 expression and apoptosis in hepatocellular carcinoma (HCC). METHODS: In situ hybridization was employed to determine caspase3 expression, and in situ end-labeling was used to detect apoptotic cells in HCC. RESULTS: Twenty one of 39 (53.8%) cases of HCC were found to express caspase3 transcripts, while 46.2% of HCC failed to express it. Adjacent non-cancerous liver tissues showed more caspase3 positiveity (87.5%, 7/8) as compared with HCC (P < 0.05). The expression of caspase3 was correlated with HCC differentiation, as 72.2% (13/18) of moderately to well differentiated HCC showed positive caspase3 transcripts, while only 38.1% of poorly differentiated HCC was caspase3 positive (P < 0.05). No relationship was found between caspase3 and tumor size or grade or metastasis, although 62.5% (5/8) of HCC with metastasis was caspase3 positive but it did not differ significantly from that without metastasis (P > 0.05). Expression of caspase3 alone did not affect the apoptosis index (AI) of HCC. AI was 7.1@1000 in caspase3-positive tumors (n = 21), as compared to 6.6@1000 (n = 18) in caspase3-negative cases (P > 0.05). CONCLUSION: Although loss of caspase3 expression may contribute to hepato-carcinogenesis, its expression may not be related to cell apoptosis in HCC.
OBJECTIVE: To investigate the relationship between caspase3 expression and apoptosis in hepatocellular carcinoma (HCC). METHODS: In situ hybridization was employed to determine caspase3 expression, and in situ end-labeling was used to detect apoptotic cells in HCC. RESULTS: Twenty one of 39 (53.8%) cases of HCC were found to express caspase3 transcripts, while 46.2% of HCC failed to express it. Adjacent non-cancerous liver tissues showed more caspase3 positiveity (87.5%, 7/8) as compared with HCC (P < 0.05). The expression of caspase3 was correlated with HCC differentiation, as 72.2% (13/18) of moderately to well differentiated HCC showed positive caspase3 transcripts, while only 38.1% of poorly differentiated HCC was caspase3 positive (P < 0.05). No relationship was found between caspase3 and tumor size or grade or metastasis, although 62.5% (5/8) of HCC with metastasis was caspase3 positive but it did not differ significantly from that without metastasis (P > 0.05). Expression of caspase3 alone did not affect the apoptosis index (AI) of HCC. AI was 7.1@1000 in caspase3-positive tumors (n = 21), as compared to 6.6@1000 (n = 18) in caspase3-negative cases (P > 0.05). CONCLUSION: Although loss of caspase3 expression may contribute to hepato-carcinogenesis, its expression may not be related to cell apoptosis in HCC.