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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

Jianping Xu1, Wei Wu2, Yao Tang1, Yanfeng Lin1, Yan Xue1, Jianda Hu3, Donghong Lin1
  • 1Department of Laboratory Medicine, School of Medical Technology and Engineering, Fujian Medical University, Fuzhou 350004, Fujian, China
  • 2Department of Laboratory Medicine, Quanzhou Medical College, Quanzhou 362011, Fujian, China
  • 3Fujian Institute of Hematology, Fujian Medical University Union Hospital, Fuzhou 350001, Fujian, China
Received: May 25, 2019Accepted: September 14, 2019Published: September 23, 2019
https://doi.org/10.18632/aging.102290

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.

Abstract

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.