CaMKII gamma regulates the viability and self-renewal of acute myeloid leukaemia stem-like cells by the Alox5/NF-kappa B pathway

文献类型： 外文期刊

第一作者： Cheng, Jiang-Hua

作者： Cheng, Jiang-Hua;Ding, Zhi-En;Cheng, Jiang-Hua;Zhang, Wen-Jing;Nie, Zheng-Chao;Ding, Bang-Sheng;Zheng, Wei-Wei;Zhu, Jun-Feng;Cui, Di;Mei, Chuan-Zhong;Song, Kai-Di;Qiang, Ping;Han, Zhong;Ding, Zhi-En

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关键词： acute myeloid leukaemia; Alox5; CaMKIIγ self‐ renewal

期刊名称：INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY （ 影响因子：2.877； 五年影响因子：2.921 ）

ISSN： 1751-5521

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收录情况： SCI

摘要： Acute myeloid leukaemia (AML) is a frequently fatal malignant disease of haematopoietic stem and progenitor cells. The molecular and phenotypic characteristics of AML are highly heterogeneous. Our previous study concluded that CaMKII gamma was the trigger of chronic myeloid leukaemia progression from the chronic phase to blast crisis, but how CaMKII gamma influences AML stem-like cells remains elusive. In this study, we found that CaMKII gamma was overexpressed in AML patients and AML cell lines, as measured by qRT-PCR and Western blot assays. Moreover, CaMKII gamma decreased when the disease was in remission. Using an shRNA lentivirus expression system, we established CaMKII gamma stable-knockdown AML cell lines and found that knockdown of CaMKII gamma inhibited the viability and self-renewal of AML stem-like cell lines. Additionally, the ratio of CD34+ AML cell lines decreased, and CaMKII gamma knockdown induced the downregulation of Alox5 levels. We further detected downstream molecules of the Alox5/NF-kappa B pathway and found that c-myc and p-I kappa B alpha decreased while total I kappa B alpha remained normal. In conclusion, our study describes a new role for CaMKII gamma as a stem-like cell marker that is highly regulated by the Alox5/NF-kappa B pathway in AML stem-like cells. CaMKII gamma can participate in the viability and self-renewal of AML stem-like cells by regulating the Alox5/NF-kappa B pathway.

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