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PRL3 enhances T-cell acute lymphoblastic leukemia growth through suppressing T-cell signaling pathways and apoptosis

E. G. Garcia, A. Veloso, M. L. Oliveira, J. R. Allen, S. Loontiens, D. Brunson, D. Do, C. Yan, R. Morris, S. Iyer, et al.
(2021) LEUKEMIA. 35. p.679-690
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Abstract
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy of thymocytes and is largely driven by the NOTCH/MYC pathway. Yet, additional oncogenic drivers are required for transformation. Here, we identify protein tyrosine phosphatase type 4 A3 (PRL3) as a collaborating oncogenic driver in T-ALL. PRL3 is expressed in a large fraction of primary human T-ALLs and is commonly co-amplified with MYC. PRL3 also synergized with MYC to initiate early-onset ALL in transgenic zebrafish and was required for human T-ALL growth and maintenance. Mass-spectrometry phosphoproteomic analysis and mechanistic studies uncovered that PRL3 suppresses downstream T-cell phosphorylation signaling pathways, including those modulated by VAV1, and subsequently suppresses apoptosis in leukemia cells. Taken together, our studies have identified new roles for PRL3 as a collaborating oncogenic driver in human T-ALL and suggest that therapeutic targeting of the PRL3 phosphatase will likely be a useful treatment strategy for T-ALL.
Keywords
Anesthesiology and Pain Medicine, Cancer Research, Hematology, NUCLEOTIDE EXCHANGE ACTIVITY, TYROSINE KINASE, FACTOR VAV1, PHOSPHATASE, RECEPTOR, EXPRESSION, METASTASIS, INVASION, NOTCH, MYC

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Citation

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MLA
Garcia, E. G., et al. “PRL3 Enhances T-Cell Acute Lymphoblastic Leukemia Growth through Suppressing T-Cell Signaling Pathways and Apoptosis.” LEUKEMIA, vol. 35, 2021, pp. 679–90, doi:10.1038/s41375-020-0937-3.
APA
Garcia, E. G., Veloso, A., Oliveira, M. L., Allen, J. R., Loontiens, S., Brunson, D., … Langenau, D. M. (2021). PRL3 enhances T-cell acute lymphoblastic leukemia growth through suppressing T-cell signaling pathways and apoptosis. LEUKEMIA, 35, 679–690. https://doi.org/10.1038/s41375-020-0937-3
Chicago author-date
Garcia, E. G., A. Veloso, M. L. Oliveira, J. R. Allen, S. Loontiens, D. Brunson, D. Do, et al. 2021. “PRL3 Enhances T-Cell Acute Lymphoblastic Leukemia Growth through Suppressing T-Cell Signaling Pathways and Apoptosis.” LEUKEMIA 35: 679–90. https://doi.org/10.1038/s41375-020-0937-3.
Chicago author-date (all authors)
Garcia, E. G., A. Veloso, M. L. Oliveira, J. R. Allen, S. Loontiens, D. Brunson, D. Do, C. Yan, R. Morris, S. Iyer, S. P. Garcia, N. Iftimia, Wouter Van Loocke, Filip Matthijssens, K. McCarthy, J. T. Barata, Franki Speleman, Tom Taghon, A. Gutierrez, Pieter Van Vlierberghe, W. Haas, J. S. Blackburn, and D. M. Langenau. 2021. “PRL3 Enhances T-Cell Acute Lymphoblastic Leukemia Growth through Suppressing T-Cell Signaling Pathways and Apoptosis.” LEUKEMIA 35: 679–690. doi:10.1038/s41375-020-0937-3.
Vancouver
1.
Garcia EG, Veloso A, Oliveira ML, Allen JR, Loontiens S, Brunson D, et al. PRL3 enhances T-cell acute lymphoblastic leukemia growth through suppressing T-cell signaling pathways and apoptosis. LEUKEMIA. 2021;35:679–90.
IEEE
[1]
E. G. Garcia et al., “PRL3 enhances T-cell acute lymphoblastic leukemia growth through suppressing T-cell signaling pathways and apoptosis,” LEUKEMIA, vol. 35, pp. 679–690, 2021.
@article{8669078,
  abstract     = {{T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy of thymocytes and is largely driven by the NOTCH/MYC pathway. Yet, additional oncogenic drivers are required for transformation. Here, we identify protein tyrosine phosphatase type 4 A3 (PRL3) as a collaborating oncogenic driver in T-ALL. PRL3 is expressed in a large fraction of primary human T-ALLs and is commonly co-amplified with MYC. PRL3 also synergized with MYC to initiate early-onset ALL in transgenic zebrafish and was required for human T-ALL growth and maintenance. Mass-spectrometry phosphoproteomic analysis and mechanistic studies uncovered that PRL3 suppresses downstream T-cell phosphorylation signaling pathways, including those modulated by VAV1, and subsequently suppresses apoptosis in leukemia cells. Taken together, our studies have identified new roles for PRL3 as a collaborating oncogenic driver in human T-ALL and suggest that therapeutic targeting of the PRL3 phosphatase will likely be a useful treatment strategy for T-ALL.}},
  author       = {{Garcia, E. G. and Veloso, A. and Oliveira, M. L. and Allen, J. R. and Loontiens, S. and Brunson, D. and Do, D. and Yan, C. and Morris, R. and Iyer, S. and Garcia, S. P. and Iftimia, N. and Van Loocke, Wouter and Matthijssens, Filip and McCarthy, K. and Barata, J. T. and Speleman, Franki and Taghon, Tom and Gutierrez, A. and Van Vlierberghe, Pieter and Haas, W. and Blackburn, J. S. and Langenau, D. M.}},
  issn         = {{0887-6924}},
  journal      = {{LEUKEMIA}},
  keywords     = {{Anesthesiology and Pain Medicine,Cancer Research,Hematology,NUCLEOTIDE EXCHANGE ACTIVITY,TYROSINE KINASE,FACTOR VAV1,PHOSPHATASE,RECEPTOR,EXPRESSION,METASTASIS,INVASION,NOTCH,MYC}},
  language     = {{eng}},
  pages        = {{679--690}},
  title        = {{PRL3 enhances T-cell acute lymphoblastic leukemia growth through suppressing T-cell signaling pathways and apoptosis}},
  url          = {{http://dx.doi.org/10.1038/s41375-020-0937-3}},
  volume       = {{35}},
  year         = {{2021}},
}
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