Decreasing of serine/threonine kinase 39 has tumour inhibiting effects on acute myeloid leukaemia by impacting the PI3K/AKT and Wnt/β-catenin signalling cascades

Serine/threonine kinase 39 (STK39) has been identified as a key regulator of tumour progression. However, whether STK39 plays a role in acute myeloid leukaemia (AML) remains undetermined. This work explored the expression and functions of STK39 in AML. STK39 was found to be overexpressed in AML and was negatively correlated with overall survival. Functionally, silencing STK39 inhibited cell proliferation, promoted cell differentiation and induced cell cycle arrest and apoptosis. The tumour inhibiting effects of STK39 downregulation were also verified by an in vivo xenograft tumour assay. Mechanistically, STK39 was closely related to the PI3K/AKT and Wnt/β-catenin signalling cascades in AML. Silencing of STK39 had suppressive effects on the PI3K/AKT and Wnt/β-catenin signalling cascades. The suppressive effect of STK39 silencing on the Wnt/β-catenin signalling cascade was significantly reversed when PI3K/AKT was reactivated. When β-catenin was re-expressed, the tumour-inhibiting effects caused by STK39 silencing were significantly eliminated. Therefore, STK39 plays a crucial role in AML and could be targeted for potential therapeutic purposes in treating AML. [Display omitted] •STK39 is overexpressed in AML and negatively related to overall survival.•Silencing of STK39 has tumour inhibiting effects on AML cells.•Silencing of STK39 decreases the phosphorylation of PI3K and AKT.•Silencing of STK39 reduces the level of phosphorylated GSK-3β and active β-catenin.•STK39 regulates AML progression via PI3K/AKT-mediated Wnt/β-catenin signalling cascade.