STK3 is a therapeutic target for a subset of acute myeloid leukemias

Research output: Contribution to journalJournal articleResearchpeer-review

Aylin Camgoz, Maciej Paszkowski-Rogacz, Shankha Satpathy, Martin Wermke, Martin V. Hamann, Malte von Bonin, Chunaram Choudhary, Stefan Knapp, Frank Buchholz

Acute myeloid leukemia (AML) is characterized by uncontrolled proliferation and accumulation of immature myeloblasts, which impair normal hematopoiesis. While this definition categorizes the disease into a distinctive group, the large number of different genetic and epigenetic alterations actually suggests that AML is not a single disease, but a plethora of malignancies. Still, most AML patients are not treated with targeted medication but rather by uniform approaches such as chemotherapy. The identification of novel treatment options likely requires the identification of cancer cell vulnerabilities that take into account the different genetic and epigenetic make-up of the individual tumors. Here we show that STK3 depletion by knock-down, knock-out or chemical inhibition results in apoptotic cells death in some but not all AML cell lines and primary cells tested. This effect is mediated by a premature activation of cyclin dependent kinase 1 (CDK1) in presence of elevated cyclin B1 levels. The anti-leukemic effects seen in both bulk and progenitor AML cells suggests that STK3 might be a promising target in a subset of AML patients.

Original languageEnglish
JournalOncoTarget
Volume9
Issue number39
Pages (from-to)25458-25473
Number of pages16
ISSN1949-2553
DOIs
Publication statusPublished - 2018

ID: 197764925