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全反式维甲酸诱导经典型霍奇金淋巴瘤B细胞表型

杜静 宫凯凯 杨丽娟 陈微微 罗丽卿

中国比较医学杂志2018,Vol.28Issue(2):46-52,7.
中国比较医学杂志2018,Vol.28Issue(2):46-52,7.DOI:10.3969.j.issn.1671-7856.2018.02.008

全反式维甲酸诱导经典型霍奇金淋巴瘤B细胞表型

Restoration of the lost B-cell phenotype in classical Hodgkin lymphoma cells by all trans-retinoic acid treatment

杜静 1宫凯凯 1杨丽娟 1陈微微 1罗丽卿2

作者信息

  • 1. 滨州医学院附属医院,肿瘤研究中心,山东 滨州 256600
  • 2. 滨州医学院附属医院,血液科,山东 滨州 256600
  • 折叠

摘要

Abstract

Objective To investigate the induction of B-cell specific phenotype in classical Hodgkin lymphoma (cHL)upon all-trans retinoic acid(ATRA)incubation. Methods To construct B-cell specific promoter(CD19, CD79a,CD79b)driven reporter plasmid with NEO cassette to realize stable transfection and selection of cHL reporter cells. To verify the intact integration by amplification of the promoter and luciferase sequences,and to functionally validate the B-cell specific promoter by ABF1 interference and luciferase assay. Repoter cells were incubated with various doses of ATRA and luciferase activity was detected at 24,48 and 72 hours. Reporter cells were treated alone or in combination with 5-Aza and ATRA followed by luciferase assay. Endogenous B-cell specific genes(CD19, CD20, CD79a and CD79b) transcription and expression levels were detected by real-time PCR and immunoblot, respectively. The expression level of CD30 antigen on Hodgkin lymphoma cell membrane upon ATRA was assessed by flow cytometry. Results ATRA treatment stimulated B-cell specific signature in cHL cells including CD19,CD79a and CD79b while down-regulated their CD30 expression. Conclusions ATRA induces B-cell phenotype deficient cHL cells to regain their B-cell transcriptional program while abolishes their Hodgkin-specific machinery.

关键词

霍奇金淋巴瘤/ATRA/B细胞表型/CD19/5-Aza

Key words

classical Hodgkin lymphoma/all-trans retinoic acid/ATRA/B-cell phenotype/CD19/5-Aza

分类

医药卫生

引用本文复制引用

杜静,宫凯凯,杨丽娟,陈微微,罗丽卿..全反式维甲酸诱导经典型霍奇金淋巴瘤B细胞表型[J].中国比较医学杂志,2018,28(2):46-52,7.

基金项目

山东省自然科学基金(ZR2016HB55) (ZR2016HB55)

烟台市科技计划(2015ZH080) (2015ZH080)

滨州医学院科研启动基金(BY2015KYQD28). (BY2015KYQD28)

中国比较医学杂志

OA北大核心CSTPCD

1671-7856

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