ArticleBlood cells, molecules & diseases2010
PRL-2 increases Epo and IL-3 responses in hematopoietic cells.
Article in Blood cells, molecules & diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Expression of phosphatase of regenerating liver-3 is associated with prognosis of Wilms' tumor.OncoTargets and therapy · 2017Article
- PRL2/PTP4A2 phosphatase is important for hematopoietic stem cell self-renewal.Stem cells (Dayton, Ohio) · 2014Article
- Molecular characterization of adipose tissue in the African elephant (Loxodonta africana).PloS one · 2014Article
- Phosphatase of regenerating liver in hematopoietic stem cells and hematological malignancies.Cell cycle (Georgetown, Tex.) · 2014Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Dual specificity protein tyrosine phosphatase PRL-2 is overexpressed in pediatric acute myeloid leukemia (AML) and is located at human chromosome 1p35, a region often rearranged or amplified in malignant lymphoma and B-cell chronic lymphocytic leukemia (B-CLL). Little is known of the significance of PRL-2 expression in hematopoietic malignancies. Herein we demonstrated that ectopic expression of PRL-2 in murine pre-B-cell line Baf3ER and mouse bone marrow cells induced key features associated with malignant progression and metastasis. PRL-2-transfected Baf3ER cells had augmented growth responses to hematopoietic growth factors Epo or IL-3 with shortened cell cycle, reduced requirement (5x) for Epo in cell survival, increased cell migration (3x), reduced cell adhesion (5x), and conversion to an immature cell morphology in association with increased expression (3x) of stem cell marker Bmi-1. When transduced into mouse bone marrow cells, PRL-2 increased Epo-induced colony formation (4x) and gave rise to larger colonies. These observations provide evidences implicating PRL-2 as a pathogenic molecule in hematopoietic malignancies and suggest its potential as a novel therapeutic target.
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Registered trials
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