可溶性CD40配体通过miR-152/SOX11信号轴调节非霍奇金淋巴瘤Raji细胞的增殖和凋亡  

Soluble CD40 ligand regulates the proliferation and apoptosis of non-Hodgkin’s lymphoma Raji cells through miR-152/SOX11 signaling axis

作　　者：苏静 梁效功 Su Jing;Liang Xiaogong(Department of Hematology,Affiliated Mianyang Hospital,Medical College of University of Electronic Science and Technology,Mianyang Central Hospital,Mianyang 621000,China)

机构地区：[1]电子科技大学医学院附属绵阳医院绵阳市中心医院血液内科,绵阳621000

出　　处：《中国组织化学与细胞化学杂志》2023年第2期161-168,共8页Chinese Journal of Histochemistry and Cytochemistry

摘　　要：目的探讨可溶性CD40配体(soluble CD40 ligand,sCD40L)基于性别决定区Y框蛋白11(SRY-related HMG box 11,SOX11)信号轴影响非霍奇金淋巴瘤Raji细胞增殖和凋亡的机制。方法对Raji细胞用sCD40L处理,或转染miR-152 mimics过表达miR-152,转染miR-152 inhibitor抑制miR-152的表达,转染SOX11 siRNA沉默SOX11的表达;用CCK-8实验检测细胞活力,流式细胞术测定细胞凋亡,Western blot检测SOX11水平,EdU染色检测细胞增殖水平,免疫组织化学染色检测Cleaved Caspase-3水平,qRT-PCR检测miR-152表达水平;应用生物信息学软件预测miR-152的靶基因,双荧光素酶报告系统鉴定miR-152与靶基因的靶向关系。结果sCD40L处理Raji细胞使其miR-152表达增多,SOX11水平降低,细胞存活率降低,细胞凋亡率升高。过表达miR-152和沉默SOX11均使Raji细胞存活率降低,细胞凋亡率升高。sCD40L处理联合抑制miR-152表达使Raji细胞存活率升高,细胞凋亡率降低,而sCD40L处理、抑制miR-152表达的同时沉默SOX11表达使则使Raji细胞存活率降低,细胞凋亡率升高。miR-152能靶向负调控SOX11。结论sCD40L通过miR-152/SOX11信号轴发挥抗非霍奇金淋巴瘤Raji细胞增殖并促进细胞凋亡的作用。Objective To investigate the mechanism of soluble CD40 ligand(sCD40L)affecting the proliferation and apoptosis of non-Hodgkin’s lymphoma Raji cells based on the signal axis of microRNA-152(miR-152)/SRY-related HMG box 11(SOX11).Methods Raji cells were treated with sCD40L,or transfected with miR-152 mimics to over-express miR-152,transfected with miR-152 inhibitor to inhibit the expression of miR-152,transfected with SOX11 siRNA to knocking-down the expression of SOX11.Cell viability was detected by CCK-8 test,cell apoptosis was detected by flow cytometry,the level of SOX11 was detected by Western blot,the level of cell proliferation was detected by EdU staining,the level of Cleaved Caspase-3 was detected by immunohistochemistry,and the level of miR-152 was detected by qRT-PCR;bioinformatics software was used to predict the target gene of miR-152,and dual luciferase reporting system was used to identify the target relationship of miR-152 to the target gene.Results The treatment with sCD40L caused increase of miR-152 expression,decrease of SOX11 level and cell survival rate,and increase of apoptosis rate of Raji cells.Both miR-152 overexpression and silencing SOX11 resulted in reduction of the survival rate and elevation of the apoptosis rate of Raji cells.The combination of sCD40L treatment and inhibition of miR-152 expression led to the increase of survival rate and decrease of the apoptosis rate of Raji cells,while the combination of sCD40L treatment,inhibition of miR-152 expression and silencing of SOX11 expression brought about decrease of the survival rate and increase of the apoptosis rate of Raji cells.miR-152 targeted SOX11,negatively regulating it.Conclusion sCD40L exerts inhibition of proliferation and promotion of apoptosis of non-Hodgkin’s lymphoma Raji cells through the miR-152/SOX11 signal axis.

关 键 词：可溶性CD40配体 性别决定区Y框蛋白11 微小RNA-152 非霍奇金淋巴瘤 凋亡 

分 类 号：R733[医药卫生—肿瘤]