Selective cyclooxygenase-2 inhibitor celecoxib could sensitize B-cell-originated lymphoma cell lines to epirubicin via down-regulation of MDR-1 mRNA and Bcl-2 mRNA expression

化范例; 王玲燕; 赵鑫

doi:10.3969/j.issn.1007-3969.2015.06.005

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Selective cyclooxygenase-2 inhibitor celecoxib could sensitize B-cell-originated lymphoma cell lines to epirubicin via down-regulation of MDR-1 mRNA and Bcl-2 mRNA expression

更新时间：2025-12-31

- Selective cyclooxygenase-2 inhibitor celecoxib could sensitize B-cell-originated lymphoma cell lines to epirubicin via down-regulation of MDR-1 mRNA and Bcl-2 mRNA expression
- China Oncology Vol. 25, Issue 6, Pages: 433-438(2015)
- 作者机构：
  
  1. 复旦大学附属金山医院血液内科,上海,201508
  2. 复旦大学附属中山医院实验研究中心,上海,200032
- 作者简介：
- 基金信息：
- DOI：10.3969/j.issn.1007-3969.2015.06.005
  CLC：
- Published Online：14 August 2015，
  
  Published：14 August 2015
- 稿件说明：
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化范例,王玲燕,赵鑫,等. 选择性COX-2抑制剂塞来昔布抑制B细胞淋巴瘤细胞株MDR-1及Bcl-2的mRNA表达并增强表柔比星的抗肿瘤作用[J]. 中国癌症杂志, 2015, 25(6): 433-438.

化范例, 王玲燕, 赵鑫. Selective cyclooxygenase-2 inhibitor celecoxib could sensitize B-cell-originated lymphoma cell lines to epirubicin via down-regulation of MDR-1 mRNA and Bcl-2 mRNA expression[J]. China Oncology, 2015, 25(6): 433-438.
化范例,王玲燕,赵鑫,等. 选择性COX-2抑制剂塞来昔布抑制B细胞淋巴瘤细胞株MDR-1及Bcl-2的mRNA表达并增强表柔比星的抗肿瘤作用[J]. 中国癌症杂志, 2015, 25(6): 433-438. DOI： 10.3969/j.issn.1007-3969.2015.06.005.

化范例, 王玲燕, 赵鑫. Selective cyclooxygenase-2 inhibitor celecoxib could sensitize B-cell-originated lymphoma cell lines to epirubicin via down-regulation of MDR-1 mRNA and Bcl-2 mRNA expression[J]. China Oncology, 2015, 25(6): 433-438. DOI： 10.3969/j.issn.1007-3969.2015.06.005.

摘要

背景与目的：部分非霍奇金淋巴瘤(non-Hodgkin’s lymphoma

NHL)具有高表达环氧合酶-2(cyclooxygenase-2，COX-2)的特征，而后者与P-糖蛋白及Bcl-2表达相关，可能导致NHL对化疗耐药。本研究旨在探讨B细胞淋巴瘤细胞株中COX-2的表达以及选择性COX-2抑制剂塞来昔布增强淋巴瘤细胞对表柔比星抗肿瘤效应的敏感性及其可能机制。方法：用荧光定量PCR(qRT-PCR)及蛋白［质］印迹法(Western blot)分别检测Raji、Jeko-1和Namalwa等淋巴瘤细胞株以及正常人外周血B细胞的COX-2表达；以梯度浓度的塞来昔布作用于淋巴瘤细胞株，CCK-8方法检测细胞增殖的抑制程度，qRT-PCR检测各细胞株MDR-1 mRNA及Bcl-2 mRNA表达的变化；表柔比星单独或联合不同浓度的塞来昔布处理Raji细胞株72 h后，CCK-8方法分析塞来昔布对表柔比星的增敏作用。结果：各淋巴瘤细胞株及正常对照外周血B细胞均不表达COX-2。塞来昔布单药即可对各淋巴瘤细胞株产生程度不同的抗增殖效应；随着塞来昔布作用浓度的增加，除Jeko-1细胞不表达MDR-1外，其余细胞株MDR-1 mRNA及Bcl-2 mRNA表达水平逐渐下降；塞来昔布明显增强表柔比星对Raji细胞的抗肿瘤活性，两者之间具有协同作用。结论：选择性COX-2抑制剂塞来昔布下调B细胞淋巴瘤细胞株的MDR-1 mRNA及Bcl-2 mRNA水平，并且增强表柔比星对淋巴瘤细胞的抗肿瘤效应。

Abstract

Background and purpose: It has been demonstrated that cyclooxygenase-2 (COX-2) is overexpressed in some subtypes of non-Hodgkin’s lymphoma (NHL)

and COX-2 correlates with the expression of P-glycoprotein and Bcl-2

which may contribute to chemotherapy-resistance in NHL. The purpose of this study was to investigate the expression of COX-2 in B-cell lymphoma cell lines and the potential mechanisms of celecoxib

a selective COX-2 inhibitor

to sensitize lymphoma cell lines to epirubicin. Methods: Quantitative fluorescent realtime poly-chain-reaction (qRT-PCR) and Western blot were employed to determine the expression of COX-2 in Raji

Jeko-1 and Namalwa cell lines

as well as in peripheral blood B cells from normal controls. Cell lines were treated with celecoxib at gradient concentrations

followed by the detection of cell viabilities by cell counting kit-8 (CCK-8). Meanwhile

the changes in expression of MDR-1 mRNA and Bcl-2 mRNA before and after celecoxib treatment were determined by qRT-PCR. Raji cells were treated with epirubicin alone or in combination with gradient concentrations of celecoxib for 72 h

then CCK-8 was used to analyze whether celecoxib sensitize Raji cells to epirubicin. Results: Neither lymphoma cell lines nor normal B cells expressed detectable COX-2 in this study. Celecoxib inhibited the proliferation of the 3 lymphoma cell lines

and the mRNA expressions of MDR-1 and Bcl-2 were decreased by celecoxib in a concentration-dependent manner

except for that MDR-1 was undetectable in Jeko-1 cells. In addition

celecoxib sensitized Raji cells to epirubicin

indicating a synergistic anti-tumor effect between the two agents. Conclusion: Selective COX-2 inhibitor celecoxib down-regulates the expressions of MDR-1 mRNA and Bcl-2 mRNA in B-cell-originated lymphoma cell lines

and sensitizes Raji cells to epirubicin.

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