中文摘要：

目的研究蛋白酪氨酸磷酸酶2（Shp2）在弥漫性大B细胞淋巴瘤（DLBCL）转化中的生物学作用及相关的信号通路调节机制。方法在Hut78细胞中,将能够特异抑制Shp2表达的si RNA（si-Shp2）转染至Hut78中,作为Shp2敲低组;转染了Scramble片段的Hut78细胞记为Hut78对照组。分别对通过细胞计数试剂盒-8（CCK-8）法检测敲低Shp2对细胞增殖的影响;Transwell实验检测敲低Shp2对细胞侵袭能力的影响;流失细胞术检测敲低Shp2对细胞凋亡能力的影响;Western blot实验分析敲低Shp2后,其相关下游效应分子的蛋白表达改变,以及Erk、Src和Akt等信号通路的激活情况。结果 Shp2敲低组的细胞增殖率和侵袭力比Hut78对照组降低,凋亡率升高,差异均有统计学意义（t分别=8.65、5.97、5.97,P均〈0.05）。Shp2敲低组细胞的c-Myc、Bcl6、Pax5、Erk和Src表达水平降低,差异具有统计学意义（t分别=7.09、6.98、5.78,6.19、7.06,P均〈0.05）。结论 Shp2在DLBCL转化中起到促进淋巴瘤细胞增殖和侵袭,抑制细胞凋亡的作用,并且Shp2的这种功能可能是通过抑制Erk和Src信号通路发挥作用。

英文摘要：

Objective To explore the biological function and detailed molecular mechanism of targeting Shp2 in diffuse large B cell lymphoma（DLBCL） transformation process. Methods Hut78 cells were divided into Shp2 knockdown group that was transfected with si RNA and control group that was transfected with scramble. The influence of knockdown Shp2 on cell proliferation was detected via CCK-8 assay, the invasion ability was detected via transwell assay and the apoptosis rate was deteceted via flow cytometry assay. The protein level and stimulation of signaling pathways including Erk, Src and Akt were detected via western blot. Results Compared with control group, the cell proliferation rate and invasive ability of Shp2 knockdown group were significantly decreased, and the apoptosis rate was significantly increased（t =8.65, 5.97,5.97, P〈0.05）.The expression level of c-Myc, Bcl-6, Pax5, Erk and Src were significantly lower in Shp2 knockdown group（t =7.09,6.98,5.78,6.19,7.06, P〈0.05）. Conclusion Shp2 plays a role in promoting proliferaton and invasion,and inhibiting apoptosis in DLBCL cells via regulating Erk and Src signaling pathway.