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血红素加氧酶-1通过JNK/c-JUN信号通路抑制急性髓系白血病细胞的凋亡。

Heme oxygenase-1 suppresses the apoptosis of acute myeloid leukemia cells via the JNK/c-JUN signaling pathway.

作者信息

Lin Xiaojing, Fang Qin, Chen Shuya, Zhe Nana, Chai Qixiang, Yu Meisheng, Zhang Yaming, Wang Ziming, Wang Jishi

机构信息

Guiyang Medical College, Guiyang 550004, China; Department of Hematology, the Affiliated Hospital of Guiyang Medical College, Guiyang 550004, China; Guizhou Provincial Laboratory of Hematopoietic Stem Cell Transplantation Center, Guiyang 550004, China.

Department of Pharmacy, the Affiliated Baiyun Hospital of Guiyang Medical College, Guiyang 550004, China.

出版信息

Leuk Res. 2015 May;39(5):544-52. doi: 10.1016/j.leukres.2015.02.009. Epub 2015 Mar 20.

DOI:10.1016/j.leukres.2015.02.009
PMID:25828744
Abstract

There are few studies on the correlation between heme oxygenase-1 (HO-1) and acute myeloid leukemia (AML). We found that HO-1 was aberrantly overexpressed in the majority of AML patients, especially in patients with acute monocytic leukemia (M5) and leukocytosis, and inhibited the apoptosis of HL-60 and U937 cells. Moreover, silencing HO-1 prolonged the survival of xenograft mouse models. Further studies demonstrated that HO-1 suppressed the apoptosis of AML cells through activating the JNK/c-JUN signaling pathway. These data indicate a molecular role of HO-1 in inhibiting cell apoptosis, allowing it to be a potential target for treating AML.

摘要

关于血红素加氧酶-1（HO-1）与急性髓系白血病（AML）之间相关性的研究较少。我们发现，HO-1在大多数AML患者中异常高表达，尤其是急性单核细胞白血病（M5）和白细胞增多症患者，并抑制HL-60和U937细胞的凋亡。此外，沉默HO-1可延长异种移植小鼠模型的生存期。进一步研究表明，HO-1通过激活JNK/c-JUN信号通路抑制AML细胞的凋亡。这些数据表明HO-1在抑制细胞凋亡中具有分子作用，使其成为治疗AML的潜在靶点。

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