Grönroos Toni, Teppo Susanna, Mehtonen Juha, Laukkanen Saara, Liuksiala Thomas, Nykter Matti, Heinäniemi Merja, Lohi Olli
Tampere Center for Child Health Research, University of Tampere and Tampere University Hospital, Tampere, Finland.
Tampere Center for Child Health Research, University of Tampere and Tampere University Hospital, Tampere, Finland.
Leuk Res. 2017 Mar;54:1-6. doi: 10.1016/j.leukres.2016.12.005. Epub 2016 Dec 26.
Cell signalling, which is often derailed in cancer, is a network of multiple interconnected pathways with numerous feedback mechanisms. Dynamics of cell signalling is intimately regulated by addition and removal of phosphate groups by kinases and phosphatases. We examined expression of members of the PTP4A family of phosphatases across acute leukemias. While expression of PTP4A1 and PTP4A2 remained relatively unchanged across diseases, PTP4A3 showed marked overexpression in ETV6-RUNX1 and BCR-ABL1 subtypes of precursor B cell acute lymphoblastic leukemia. We show that PTP4A3 is regulated by the ETV6-RUNX1 fusion, but noticed no marked impact on cell viability either after PTP4A3 silencing or treatment with a PTP4A3 inhibitor. Regulation of PTP4A3 expression is altered in specific subgroups of acute leukemias and this is likely brought about by expression of the aberrant fusion genes.
细胞信号传导在癌症中常常发生紊乱，它是一个由多个相互连接的途径以及众多反馈机制组成的网络。细胞信号传导的动态过程受到激酶和磷酸酶对磷酸基团的添加和去除的密切调控。我们研究了磷酸酶PTP4A家族成员在急性白血病中的表达情况。虽然PTP4A1和PTP4A2的表达在各种疾病中相对保持不变，但PTP4A3在前体B细胞急性淋巴细胞白血病的ETV6 - RUNX1和BCR - ABL1亚型中显著过表达。我们发现PTP4A3受ETV6 - RUNX1融合基因调控，但在PTP4A3沉默或用PTP4A3抑制剂处理后，均未发现对细胞活力有明显影响。PTP4A3表达的调控在急性白血病的特定亚组中发生改变，这可能是由异常融合基因的表达引起的。
