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分析 T 细胞急性淋巴细胞白血病患者中 BCL11B 基因及其亲属的表达模式。

Analysis of the expression pattern of the BCL11B gene and its relatives in patients with T-cell acute lymphoblastic leukemia.

机构信息

Institute of Hematology, Medical College, Jinan University, and Department of Hematology, Guangdong General Hospital, Guangzhou, 510632, PR China.

出版信息

J Hematol Oncol. 2010 Nov 16;3(1):44. doi: 10.1186/1756-8722-3-44.

DOI:10.1186/1756-8722-3-44
PMID:21080944
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2992472/
Abstract

BACKGROUND

In a human T-cell acute lymphoblastic leukemia (T-ALL) cell line (Molt-4), siRNA-mediated suppression of BCL11B expression was shown to inhibit proliferation and induce apoptosis, functions which may be related to genes involved in apoptosis (such as TNFSF10 and BCL2L1) and TGF-β pathways (such as SPP1and CREBBP).

METHODS

The expression levels of the above mentioned genes and their correlation with the BCL11B gene were analyzed in patients with T-ALL using the TaqMan and SYBR Green I real-time polymerase chain reaction technique.

RESULTS

Expression levels of BCL11B, BCL2L1, and CREBBP mRNA in T-ALL patients were significantly higher than those from healthy controls (P<0.05). In T-ALL patients, the BCL11B expression level was negatively correlated with the BCL2L1 expression level (rs=-0.700; P<0.05), and positively correlated with the SPP1 expression level (rs=0.683; P<0.05). In healthy controls, the BCL11B expression level did not correlate with the TNFSF10, BCL2L1, SPP1, or CREBBP expression levels.

CONCLUSIONS

Over-expression of BCL11B might play a role in anti-apoptosis in T-ALL cells through up-regulation of its downstream genes BCL2L1 and CREBBP.

摘要

背景

在人类 T 细胞急性淋巴细胞白血病(T-ALL)细胞系(Molt-4)中,siRNA 介导的 BCL11B 表达抑制可抑制增殖并诱导细胞凋亡,这些功能可能与凋亡相关基因(如 TNFSF10 和 BCL2L1)和 TGF-β 途径(如 SPP1 和 CREBBP)有关。

方法

采用 TaqMan 和 SYBR Green I 实时聚合酶链反应技术分析 T-ALL 患者上述基因的表达水平及其与 BCL11B 基因的相关性。

结果

T-ALL 患者的 BCL11B、BCL2L1 和 CREBBP mRNA 表达水平明显高于健康对照组(P<0.05)。在 T-ALL 患者中,BCL11B 表达水平与 BCL2L1 表达水平呈负相关(rs=-0.700;P<0.05),与 SPP1 表达水平呈正相关(rs=0.683;P<0.05)。在健康对照组中,BCL11B 表达水平与 TNFSF10、BCL2L1、SPP1 或 CREBBP 表达水平无相关性。

结论

BCL11B 的过表达可能通过上调其下游基因 BCL2L1 和 CREBBP 在 T-ALL 细胞中发挥抗凋亡作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f93/2992472/b5b78fc27183/1756-8722-3-44-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f93/2992472/307631dc1f15/1756-8722-3-44-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f93/2992472/5ac19d642961/1756-8722-3-44-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f93/2992472/3045d612d47f/1756-8722-3-44-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f93/2992472/b5b78fc27183/1756-8722-3-44-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f93/2992472/307631dc1f15/1756-8722-3-44-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f93/2992472/5ac19d642961/1756-8722-3-44-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f93/2992472/3045d612d47f/1756-8722-3-44-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f93/2992472/b5b78fc27183/1756-8722-3-44-4.jpg

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