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目的 探讨STAT3磷酸化对胃MALT淋巴瘤细胞凋亡的调控作用。方法 采用SP免疫组织化学方法检测了 45例胃MALT淋巴瘤细胞及 13例滤泡型淋巴结反应性增生病 (RH)的p -STAT3、促凋亡基因 /蛋白fas和抗凋亡基因 /蛋白bcl-2的表达。结果 p -STAT3、fas及bcl-2蛋白在胃MALT淋巴瘤细胞中均呈过度表达 (阳性率分别为 64 .4%、60 .0 %和 66.7% ) ;低度恶性组的fas蛋白阳性信号强度明显低于高度恶性组 (P <0 .0 5 ) ,而bcl-2蛋白则明显高于高度恶性组 (P <0 .0 5 ) ,在低度与高度恶性组间的p -STAT3阳性表达强度无明显差异 (P >0 .0 5 ) ;p -STAT3与fas蛋白在胃MALT淋巴瘤细胞中的阳性表达呈明显的负相关 (r=-0 .6791,P <0 .0 5 ) ,而与bcl -2蛋白的阳性表达则呈明显的正相关 (r=0 .72 3 1,P <0 .0 5 )。结论 STAT3活化可能通过抑制细胞凋亡导致胃MALT淋巴瘤细胞的恶性转化及高增殖性 ,并在其演进中起重要作用
Objective To investigate the role of STAT3 phosphorylation in the apoptosis of gastric MALT lymphoma cells. Methods SP immunohistochemistry was used to detect the expression of p-STAT3, apoptosis-promoting genes / protein fas and anti-apoptotic gene / protein bcl in 45 gastric MALT lymphoma cells and 13 follicular lymph node reactive hyperplasia (RH) -2 expression. Results The expressions of p-STAT3, fas and bcl-2 protein were overexpressed in gastric MALT lymphoma cells (positive rates were 64.4%, 60.0% and 66.7% respectively) The intensity of bcl-2 protein was significantly lower than that of the highly malignant group (P <0.05), but lower than that of the highly malignant group (P <0.05) The expression of pSTST3 and fas protein in gastric MALT lymphoma showed a significant negative correlation (r = -0.6671, P <0.05) , But positively correlated with the expression of bcl-2 protein (r = 0.7231, P <0.05). Conclusion STAT3 activation may induce malignant transformation and hyperproliferation of gastric MALT lymphoma cells by inhibiting apoptosis, and play an important role in its evolution