A loss-of-function genetic screening reveals synergistic targeting of AKT/mTOR and WTN/β-catenin pathways for treatment of AML with high PRL-3 phosphatase

• Main Authors: Zhou, J, Toh, S.H.-M, Chan, Z.-L, Quah, J.Y, Chooi, J.-Y, Tan, T.Z, Chong, P.S.Y, Zeng, Q, Chng, W.-J
• Other Authors: CANCER SCIENCE INSTITUTE OF SINGAPORE
• Format: Article
• Published: 2020
• Subjects: beta catenin; mammalian target of rapamycin; oncoprotein; PRL 3 phosphatase; protein kinase B; short hairpin RNA; unclassified drug; Wnt protein; MTOR protein, human; protein tyrosine phosphatase; PTP4A3 protein, human; target of rapamycin kinase; tumor protein; acute myeloid leukemia; acute myeloid leukemia cell line; Akt/mTOR signaling; animal experiment; animal model; Article; bone marrow cell; cancer prognosis; cancer survival; cell assay; controlled study; enzyme inhibition; gene library; genetic screening; human; human cell; in vitro study; in vivo study; mouse; nonhuman; protein expression; protein protein interaction; protein targeting; upregulation; Wnt beta catenin signaling; Wnt signaling; animal; female; genetics; metabolism; nonobese diabetic mouse; procedures; SCID mouse; Animals; beta Catenin; Female; Genetic Testing; Humans; Leukemia, Myeloid, Acute; Mice; Mice, Inbred NOD; Mice, SCID; Neoplasm Proteins; Protein Tyrosine Phosphatases; Proto-Oncogene Proteins c-akt; TOR Serine-Threonine Kinases; Wnt Signaling Pathway
• Online Access: https://scholarbank.nus.edu.sg/handle/10635/178101
• Institution: National University of Singapore

10.1186/s13045-018-0581-9