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Analysis of the expression pattern of the BCL11B gene and its relatives in patients with T-cell acute lymphoblastic leukemia
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  • 作者：Xin Huang (1) (2)
    Shaohua Chen (1)
    Qi Shen (1)
    Lijian Yang (1)
    Bo Li (1)
    Liye Zhong (1) (2)
    Suxia Geng (2)
    Xin Du (2)
    Yangqiu Li (1) (3)
  • 刊名：Journal of Hematology & Oncology
  • 出版年：2010
  • 出版时间：December 2010
  • 年：2010
  • 卷：3
  • 期：1
  • 全文大小：1004KB
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  • 作者单位：Xin Huang (1) (2)
    Shaohua Chen (1)
    Qi Shen (1)
    Lijian Yang (1)
    Bo Li (1)
    Liye Zhong (1) (2)
    Suxia Geng (2)
    Xin Du (2)
    Yangqiu Li (1) (3)

    1. Institute of Hematology, Medical College, Jinan University, 510632, Guangzhou, PR China
    2. Department of Hematology, Guangdong General Hospital (Guangdong Academy of Medical Sciences), 510080, Guangzhou, PR China
    3. Key Laboratory for Regenerative Medicine of Ministry of Education, Jinan University, 510632, Guangzhou, PR China
  • ISSN：1756-8722
文摘
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 SPP1 and 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 (r s = -0.700; P < 0.05), and positively correlated with the SPP1 expression level (r s = 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.

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