醛酮还原酶家族1成员B10(AKR1B10)通过激活Wnt/β-catenin通路促进乳腺癌细胞增殖  

AKR1B10 promotes proliferation of breast cancer cells by activating Wnt/β-catenin pathway

作　　者：屈佳肴 刘香婷 李佳[2] 龚珂 段丽丽[2] 罗文娜 罗迪贤 QU Jiayao;LIU Xiangting;LI Jia;GONG Ke;DUAN Lili;LUO Wenna;LUO Dixian(First School of Clinical Medicine,Southern Medical University,Guangzhou 510000;Translational Medicine Institute,First People’s Hospital of Chenzhou,Chenzhou 423000;Department of Laboratory,Donghua Hospital Affiliated to Sun Yat-sen University,Dongguan 523000;First Affiliated Hospital of Jinan University,Guangzhou 510000,China)

机构地区：[1]南方医科大学第一临床医学院,广东广州510000 [2]郴州市第一人民医院转化医学研究所,湖南郴州423000 [3]中山大学附属东华医院检验科,广东东莞523000 [4]暨南大学附属第一医院检验科,广东广州510000

出　　处：《细胞与分子免疫学杂志》2019年第12期1094-1100,共7页Chinese Journal of Cellular and Molecular Immunology

基　　金：湖南省自然科学杰出青年基金(2018JJ1021);湖南省自然科学基金(2019JJ50022);湖南省卫生健康委科研计划课题(B20180266,B2019001);郴州市科技计划项目(jsyf2017023,zdyf201837)。

摘　　要：目的探讨醛酮还原酶家族1成员B10(AKR1B10)对乳腺癌细胞增殖的影响及其机制。方法在乳腺癌MCF-7细胞过表达AKR1B10、在BT-20细胞敲低AKR1B10,分别建立过表达以及敲低细胞系。利用CCK-8增殖实验检测过表达与敲低AKR1B10对乳腺癌细胞增殖的影响。实时荧光定量PCR检测乳腺癌组织及配对正常组织AKR1B10 mRNA水平,Western blot法检测乳腺癌组织、过表达及敲低AKRB10的乳腺癌细胞AKR1B10、β联蛋白(β-catenin)、细胞周期蛋白D1(cyclin D1)、存活蛋白(survivin)、c-Myc的蛋白水平。结果乳腺癌组织AKR1B10表达增加。过表达AKR1B10后,MCF-7乳腺癌细胞增殖加快,β-catenin、cyclin D1、c-Myc、survivin蛋白表达增加;敲低AKR1B10后,BT-20乳腺癌细胞增殖变慢,β-catenin、cyclin D1、c-Myc、survivin蛋白表达下降。结论AKR1B10在乳腺癌中高表达并通过激活Wnt/β-catenin信号通路促进乳腺癌细胞增殖。Objective To investigate the effect of aldosterone reductase family 1 member B10(AKR1B10) on breast cancer cell proliferation and its mechanism. Methods AKR1B10 was overexpressed in MCF-7 cells and knocked down in BT-20 cells to establish both AKR1B10 overexpression and knockdown cell lines. The effect of AKR1B10 overexpression and knockdown on breast cancer cell proliferation was examined by CCK-8 assay. Real-time quantitative PCR was performed to detect AKR1B10 mRNA levels in breast cancer tissues and paired normal tissues. Western blot analysis was used to determine the protein levels of AKR1B10, β-catenin, cyclin D1, survivin, c-myc in breast cancer tissues and AKR1B10 overexpression/knockdown breast cancer cell lines. Results The expression of AKR1B10 was higher in breast cancer tissues. With AKR1B10 overexpression in MCF-7 cells, cell proliferation was promoted, and the expression levels of β-catenin, cyclin D1, c-myc and survivin were elevated. Meanwhile, knockdown of AKR1B10 in BT-20 breast cancer cells reduced cell proliferation and the expression levels of β-catenin, cyclin D1, c-myc and survivin. Conclusion AKR1B10 is highly expressed in breast cancer and promotes breast cancer cell proliferation by activating Wnt/β-catenin signaling pathway.

关 键 词：乳腺癌 醛-酮还原酶家族1成员B10(AKR1B10) WNT信号通路 细胞增殖 

分 类 号：Q279[生物学—细胞生物学] R737.9[医药卫生—肿瘤]