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    Overexpressing TPTE2 (TPIP), a homolog of the human tumor suppressor gene PTEN, rescues the abnormal phenotype of the PTEN-/- mutant

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    Author
    Lusche, D.F.
    Buchele, E.C.
    Russell, K.B.
    Date
    2018
    Journal
    Oncotarget
    Publisher
    Impact Journals LLC
    Type
    Article
    
    Metadata
    Show full item record
    See at
    https://dx.doi.org/10.18632/oncotarget.24941
    Abstract
    One possible approach to normalize mutant cells that are metastatic and tumorigenic, is to upregulate a functionally similar homolog of the mutated gene. Here we have explored this hypothesis by generating an overexpressor of TPTE2 (TPIP), a homolog of PTEN, in PTEN-/- mutants, the latter generated by targeted mutagenesis of a human epithelial cell line. Overexpression of TPTE2 normalized phenotypic changes associated with the PTEN mutation. The PTEN-/--associated changes rescued by overexpressing TPTE2 included 1) accelerated wound healing in the presence or absence of added growth factors (GFs), 2) increased division rates on a 2D substrate in the presence of GFs, 3) adhesion and viability on a 2D substrate in the absence of GFs, 4) viability in a 3D Matrigel model in the absence of GFs and substrate adhesion 5) loss of apoptosis-associated annexin V cell surface binding sites. The results justify further exploration into the possibility that upregulating TPTE2 by a drug may reverse metastatic and tumorigenic phenotypes mediated in part by a mutation in PTEN. This strategy may also be applicable to other tumorigenic mutations in which a homolog to the mutated gene is present and can substitute functionally. Copyright Lusche et al.
    Sponsors
    Research in the Soll laboratory was supported by the Developmental Studies Hybridoma Bank, a self-funded National Resource created by the NIH. Research in the Vitolo lab was supported by NIH grant K01-CA166567.
    Keyword
    Cancer cell rescue
    TPTE2 TPIP
    Transmembrane phosphatase
    Tumor suppressor
    Wound healing
    Identifier to cite or link to this item
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-85045855036&doi=10.18632%2foncotarget.24941&partnerID=40&md5=cdcbf5c7087c3303109a9e51a28aa8af; http://hdl.handle.net/10713/9307
    ae974a485f413a2113503eed53cd6c53
    10.18632/oncotarget.24941
    Scopus Count
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