TY - JOUR
T1 - Phosphatase of regenerating liver in hematopoietic stem cells and hematological malignancies
AU - Kobayashi, Michihiro
AU - Chen, Sisi
AU - Gao, Rui
AU - Bai, Yunpeng
AU - Zhang, Zhong Yin
AU - Liu, Yan
N1 - Funding Information:
This work was supported by National Institutes of Health (R01 CA69202 to Z- YZ), Department of Defense (Career Development Award CA120373 to YL), St. Baldrick’s Foundation (Scholar Award to YL), Elsa Pardee Foundation (Research Fund to YL), American Cancer Society (Institutional Research Grants to YL and MK) and Alex’s Lemonade Stand Foundation (Research Fund to YL).
Publisher Copyright:
© 2014 Taylor & Francis Group, LLC.
PY - 2014
Y1 - 2014
N2 - The phosphatases of regenerating liver (PRLs), consisting PRL1, PRL2 and PRL3, are dual-specificity protein phosphatases that have been implicated as biomarkers and therapeutic targets in several solid tumors. However, their roles in hematological malignancies are largely unknown. Recent findings demonstrate that PRL2 is important for hematopoietic stem cell self-renewal and proliferation. In addition, both PRL2 and PRL3 are highly expressed in some hematological malignancies, including acute myeloid leukemia (AML), chronic myeloid leukemia (CML), multiple myeloma (MM) and acute lymphoblastic leukemia (ALL). Moreover, PRL deficiency impairs the proliferation and survival of leukemia cells through regulating oncogenic signaling pathways. While PRLs are potential novel therapeutic targets in hematological malignancies, their exact biological function and cellular substrates remain unclear. This review will discuss how PRLs regulate hematopoietic stem cell behavior, what signaling pathways are regulated by PRLs, and how to target PRLs in hematological malignancies. An improved understanding of how PRLs function and how they are regulated may facilitate the development of PRL inhibitors that are effective in cancer treatment.
AB - The phosphatases of regenerating liver (PRLs), consisting PRL1, PRL2 and PRL3, are dual-specificity protein phosphatases that have been implicated as biomarkers and therapeutic targets in several solid tumors. However, their roles in hematological malignancies are largely unknown. Recent findings demonstrate that PRL2 is important for hematopoietic stem cell self-renewal and proliferation. In addition, both PRL2 and PRL3 are highly expressed in some hematological malignancies, including acute myeloid leukemia (AML), chronic myeloid leukemia (CML), multiple myeloma (MM) and acute lymphoblastic leukemia (ALL). Moreover, PRL deficiency impairs the proliferation and survival of leukemia cells through regulating oncogenic signaling pathways. While PRLs are potential novel therapeutic targets in hematological malignancies, their exact biological function and cellular substrates remain unclear. This review will discuss how PRLs regulate hematopoietic stem cell behavior, what signaling pathways are regulated by PRLs, and how to target PRLs in hematological malignancies. An improved understanding of how PRLs function and how they are regulated may facilitate the development of PRL inhibitors that are effective in cancer treatment.
KW - Hematological malignancy and therapeutic target
KW - Hematopoietic stem cell
KW - Oncogenic signaling
KW - PRL
KW - PTP4A
KW - Self-renewal
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U2 - 10.4161/15384101.2014.954448
DO - 10.4161/15384101.2014.954448
M3 - Article
C2 - 25486470
AN - SCOPUS:84964313604
SN - 1538-4101
VL - 13
SP - 2827
EP - 2835
JO - Cell Cycle
JF - Cell Cycle
IS - 18
ER -
