Please use this identifier to cite or link to this item: https://doi.org/10.1158/1541-7786.MCR-16-0275-T
Title: LIN28B Activation by PRL-3 Promotes Leukemogenesis and a Stem Cell-like Transcriptional Program in AML
Authors: Zhou, Jianbiao 
Chan, Zit-Liang
Bi, Chonglei
Lu, Xiao
Chong, Phyllis SY 
Chooi, Jing-Yuan 
Cheong, Lip-Lee
Liu, Shaw-Cheng
Ching, Ying Qing 
Zhou, Yafeng
Osato, Motomi
Tan, Tuan Zea 
Ng, Chin Hin 
Ng, Siok-Bian 
Wang, Shi 
Zeng, Qi 
Chng, Wee-Joo 
Keywords: Science & Technology
Life Sciences & Biomedicine
Oncology
Cell Biology
ACUTE MYELOID-LEUKEMIA
MONOCLONAL-ANTIBODIES
MICRORNA BIOGENESIS
REGENERATING LIVER
PHOSPHATASE PRL-3
CANCER
METASTASIS
EXPRESSION
PROTEIN
TARGET
Issue Date: 1-Mar-2017
Publisher: AMER ASSOC CANCER RESEARCH
Citation: Zhou, Jianbiao, Chan, Zit-Liang, Bi, Chonglei, Lu, Xiao, Chong, Phyllis SY, Chooi, Jing-Yuan, Cheong, Lip-Lee, Liu, Shaw-Cheng, Ching, Ying Qing, Zhou, Yafeng, Osato, Motomi, Tan, Tuan Zea, Ng, Chin Hin, Ng, Siok-Bian, Wang, Shi, Zeng, Qi, Chng, Wee-Joo (2017-03-01). LIN28B Activation by PRL-3 Promotes Leukemogenesis and a Stem Cell-like Transcriptional Program in AML. MOLECULAR CANCER RESEARCH 15 (3) : 294-303. ScholarBank@NUS Repository. https://doi.org/10.1158/1541-7786.MCR-16-0275-T
Abstract: PRL-3 (PTP4A3), a metastasis-associated phosphatase, is also upregulated in patients with acute myeloid leukemia (AML) and is associated with poor prognosis, but the underlying molecular mechanism is unknown. Here, constitutive expression of PRL-3 in human AML cells sustains leukemogenesis in vitro and in vivo. Furthermore, PRL-3 phosphatase activity dependently upregulates LIN28B, a stem cell reprogramming factor, which in turn represses the let-7 mRNA family, inducing a stem cell-like transcriptional program. Notably, elevated levels of LIN28B protein independently associate with worse survival in AML patients. Thus, these results establish a novel signaling axis involving PRL-3/LIN28B/let-7, which confers stem cell-like properties to leukemia cells that is important for leukemogenesis. Implications: The current study of fers a rationale for targeting PRL-3 as a therapeutic approach for a subset of AML patients with poor prognosis.
Source Title: MOLECULAR CANCER RESEARCH
URI: https://scholarbank.nus.edu.sg/handle/10635/207398
ISSN: 15417786
15573125
DOI: 10.1158/1541-7786.MCR-16-0275-T
Appears in Collections:Staff Publications
Elements

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
Zhou J. Mol Cancer Res 2016. LIN28B in AML.pdfPublished version1.58 MBAdobe PDF

CLOSED

Published

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.