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  • Title: Live kinase B1 maintains CD34+CD38- AML cell proliferation and self-renewal.
    Author: Wang H, Wang X, Xin N, Qi L, Liao A, Yang W, Liu Z, Zhao C.
    Journal: Mol Cell Biochem; 2017 Oct; 434(1-2):25-32. PubMed ID: 28397012.
    Abstract:
    Live kinase B1 (LKB1) has been recognized as a tumor suppressor in many human cancers; however, LKB1 maintains self-renewal of hematopoietic stem cells (HSCs). The existence of leukemia stem cells (LSCs) is responsible for drug resistance and leukemia relapse. In acute myeloid leukemia (AML), CD34+CD38- fraction is the most enriched compartment for LSCs. We found that LKB1 was upregulated in CD34+CD38- AML cells. LKB1 downregulation suppressed the long-term proliferation of CD34+CD38- AML cells, induced CD34+CD38- AML cells into G2/M phase, and enhanced the sensitivity of CD34+CD38- AML cells to chemotherapy. Furthermore, LKB1 downregulation in CD34+CD38- AML cells inhibited tumor formation in NOD-SCID mice. Downregulation of LKB1 gene makes LSCs partly loose the characters as stem cells. Gene expression microarray showed that MAPK/ERK pathway was implicated in the regulation of CD34+CD38- AML cell proliferation by LKB1. Together, these findings demonstrate that LKB1 plays an important role in the maintenance of LSCs, which may be responsible for drug resistance and AML relapse.
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