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Purpose of glial cell line-derived neurotrophic factor GDNF and its receptor Ret in salivary adenoid cystic carcinoma (ACC) and perineural invasion (PNI) in the role and possible mechanisms. Explore the salivary gland ACC and MMP-9, NF-κB, VEGF, integrin β1, Bcl-xL matrix degradation, angiogenesis, adhesion ability changes, changes in the ability of the anti-apoptotic role and impact of ACC perineural invasion possible mechanisms. Method 1 application of immunohistochemistry SP method in 42 patients the ACC, 5 cases of acinar cell carcinoma, 5 cases of normal salivary gland tissue of GDNF, Ret expression and 42 cases of ACC in MMP-9, NF-κB, VEGF, integrin β1, to detect the expression of Bcl-xL. 2 All statistics were applied the SPSS16.0 software processing analysis, counting χ2 test or Fisher exact test was used to compare data sets, more than two sets of count data compared using one-way ANOVA (ANVOA), the correlation between the two groups ranked data The analyzes were performed using the Spearman rank correlation test. P lt; 0.05 indicates that the difference was statistically significant. Results 1 GDNF positive expression in the ACC the cytoplasm of the tumor cells and the tumor around the nerve fibers, but was not expressed in the acinar cell carcinoma and normal acinar. Ret in ACC tumor cell cytoplasm positive expression of nerve fibers in the weak or no expression in acinar cell carcinoma and normal acinar expression. GDNF and Ret positive expression rate was 69.05% (29/42), 69.05% (29/42), the both expression was positively correlated (r = 0.554, P = 0.000). GDNF expression in clinical stage early group and the late group positive expression rate of 38.46% (5/13), 82.76% (24/29), the difference was statistically significant (P = 0.012), the expression of GDNF in tubular type, cribriform enrich the type of positive expression rate was 91.67% (11/12), 45.00% (9/20), 90.00% (9/10), the difference was statistically significant (P = 0.006). 2 NF-κB, MMP-9, integrated cable β1 positive expression of both in ACC tumor cell cytoplasm, and occasionally NF-κB expression in the nucleus, the positive expression rate of 69.05% (29/42), 66.67% ( 28/42), 61.90% (26/42). Stromal cells surrounding the tumor MMP-9 also has a small amount of expression. GDNF, NF-κB, MMP-9, integration of β1 expression the PNI group and non-PNI group difference was statistically significant (P values ??were 0.000,0.005,0.0 I 1,0.0011. GDNF and NF-κB, MMP -9, integrated cable β1 expression was positive (r = 0.443, P = 0.003; r = 0.401, P = 0.009; r = 0.535, P = 0.000) MMP-9 in, integration of β1 and NF-κB expression was positively related (r = 0.501, P = 0.001; r = 0.429, P = 0.005). expression of MMP-9 expression and integration prime β1, the expression of VEGF was positive related (r = 0.381, P = 0.013; r = 0.652, P = 0.000 ) integrated cable β1, MMP-9, NF-κB expression in early clinical stage group late positive expression rate of 30.77% (4/13), 75.86% (22/29); 38.46% (5 / 13), 79.31% (23/29); 38.46% (5/13), 82.76% (24/29), the difference was statistically significant (P = bit is for 0.015,0.025,0.012). 3 of VEGF of Bcl- xL was bloody expression of in ACC tumor cell cytoplasm, the positive expression rate was 59.52% (25/42), 57.14% (24/42) of VEGF, Bcl-xL expression the PNI group and non-PNI group differences between statistically significant (P = 0.011, P = 0.000) of GDNF and VEGF, Bcl-xL expression correlation (P = 0.124, P = 0.700). VEGF, Bcl-xL and NF-κB expression was positively correlated (r = 0.392, P = 0.010; r = 0.357, P = 0.0201 expression of VEGF positive expression rate of clinical stage early group and the late group were 23.08% (3/13), 75.86% (22/29), the difference statistically significant (P = 0.004). 4 of GDNF expression and accompanied by neurological symptoms group ACC with and without between neurological symptoms group ACC difference was statistically significant (P = 0.033) Conclusion 1 GDNF and its receptor Ret in the ACC in the high expression, GDNF in peripheral nerve tissue, high expression, suggesting that the ACC in the presence of GDNF autocrine of GDNF and Ret perineural invasion in the ACC may play an important role of GDNF involved in NF-κB activation and MMP-9, integrin β1 transcription and expression of integrin β1 conducive to tumor cell adhesion in tumor surrounding matrix, MMP-9 degradation around the tumor matrix, the two together to change the tumor microenvironment promote the ACC cell invasion nerve. angiogenesis and tumor cell resistance to apoptosis capabilities help ACC perineural invasion occurred and progress, but the statistical correlation between the ability to increase the expression of GDNF, there may be other factors involved in tumor angiogenesis, anti-apoptotic ability addicted neural invasion. 4 of GDNF expression may be associated with ACC patients with neurological symptoms
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