Research Paper Volume 11, Issue 18 pp 7817—7829
PRL-3 exerts oncogenic functions in myeloid leukemia cells via aberrant dephosphorylation of stathmin and activation of STAT3 signaling
- 1 Department of Laboratory Medicine, School of Medical Technology and Engineering, Fujian Medical University, Fuzhou 350004, Fujian, China
- 2 Department of Laboratory Medicine, Quanzhou Medical College, Quanzhou 362011, Fujian, China
- 3 Fujian Institute of Hematology, Fujian Medical University Union Hospital, Fuzhou 350001, Fujian, China
received: May 25, 2019 ; accepted: September 14, 2019 ; published: September 23, 2019 ;https://doi.org/10.18632/aging.102290
How to Cite
Copyright © 2019 Xu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PRL-3, an oncogenic dual-specificity phosphatase, is overexpressed in 50% of acute myeloid leukemia patients. Stathmin has been identified as a downstream target of PRL-3 in colorectal cancer. However, the correlation between PRL-3 and stathmin in myeloid leukemia is unclear. In this study, we revealed the positive correlation between PRL-3 and stathmin in myeloid leukemia. Knockdown of the PRL-3 gene by shRNA reduced the expression of downstream stathmin, suppressed cell proliferation, induced G2/M arrest and cell apoptosis, and inhibited migration and invasion in myeloid leukemia cells. Moreover, our study was the first to provide evidence that silencing PRL-3 increased the phosphorylation level in Ser16, Ser25, Ser38, and Ser63 of stathmin, and in turn inhibited the STAT3 and STAT5 signaling in myeloid leukemia cells. This evidence points to a promoted role for PRL-3 in the progression of myeloid leukemia, and PRL-3 could be a possible new treatment target.