| Objective:To investigate the expression of Polycomb group proteins(BMI-1、EZH2),cell cycle proteins(Ki-67、p53、p16),VEGF in salivary gland adenoid cystic careinoma(ACC) tissue,and to explore the relationship with the clinical,pathological and the role in the pathogenesis of ACC.Methods:1. Totally42ACCs,5-normal salivary gland tissues were included in the present study. Expression of the VEGF,cell cycle proteins Ki-67、p53and p16, together with the Polycomb group(PcG) proteins BMI-1and EZH2was investigated immunohistochemically47formalin-fixed,paraffin-embedded primary ACCs in relation to tumour characteristics.2. All data analyszs by Chi Square test、Spearman Correlation were Performed on SPSS16.0software.P values less than0.05were considered statistically significant.Results:1. EZH2、BMI-1were both positively expressed in ACC cell nucleus.The positive expression rate was66.67%(28/42)、57.14%(24/42),respectively.The positive expression rate difference between early clinical staging30.00%(3/10) and advanced clinical staging78.12%(25/32) of expression of EZH2was statistically significant (P=0.015,P<0.05), and so was the positive expression rate difference between solid92.85%(13/14) and cribriform/tubular53.57%(15/28) of expression of EZH2(P=0.028,P<0.05).The positive expression rate difference between solid(85.71%,12/14) and cribriform/tubular(42.85%,12/28) of expression of BMI-1(P=0.021,P<0.05).2. Ki-67、p53were both positively expressed in ACC cell nucleus.The positive expression rate was78.57%(33/42)、59.52%(25/42),respectively. p16was positively expressed in cell nucleus.The positive expression rate of p16in normal salivary gland and ACC were100.00%(5/5) and28.57%(12/42) respectively.The positive expression rate difference between early clinical staging(40.00%,4/10) and advanced clinical staging(90.62%,29/32) of expression of Ki-67was statistically significant (P=0.003,P<0.05),and so was the positive expression rate difference between solid and cribriform/tubular of expression of Ki-67(P=0.046,P<0.05).The positive expression rate difference between solid(85.71%,12/14) and cribriform/tubular (46.42%,13/28) of expression of p53(P=0.035,P<0.05).The positive expression rate difference between early clinical staging(60.00%,6/10) and advanced clinical staging (18.75%,6/32) of expression of p16was statistically significant (P=0.034,P<0.05).3. VEGF was positively expressed in ACC cell cytoplasm, the positive expression rate was61.90%(26/42).The positive expression rate difference between solid (92.85%,13/14) and cribriform/tubular (46.42%,13/28) of expression of VEGF (P=0.010,P<0.05).The positive expression rate difference between early clinical staging30.00%(3/10) and advanced clinical staging71.85%(23/32) of expression of VEGF was statistically significant (P=0.045,P<0.05).4. Expression of BMI-1、Ki-67、p53、VEGF were correlated to that of EZH2(r=0.510,P=0.001;r=0.492,P=0.001;r=0.652,P=0.000;r=0.381,P=0.013,respectively). Expression of Ki-67was correlated with p53(r=0.515,P=0.000).Expression of Ki-67. p53were correlated to that of VEGF(r=0.427,P=0.005;r=0.752,P=0.000).Conclusions:1. EZH2and BMI-1were both positively expressed in ACC nucleus, indicating that EZH2and BMI-1involved in the early biological event of ACC.2. Ki-67and p53were positively expressed in ACC,p16was negatively expressed in ACC.Cell cycle protein expression in ACC is disturbed compared to normal salivary gland tissue,excessive proliferation of tumor cells, and eventually lead to the formation of tumor.3. EZH2can affect expression of cell cycle proteins through participate cell cycle regulation,indicating that EZH2and cell cycle proteins may play both independent and collaborative effects in the process of clinic pathologic of ACC.4. Angiogenesis contribute to the development and progression of ACC.The increase in endothelial EZH2is a direct result of VEGF stimulation by a paracrine circuit that promotes angiogenesis by methylating and silencing vasohibinl (vashl). |
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