Science Signal: Rac1 does not rely on PI3K and GTPase-mediated MET-driven anchornon cell growth
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Last Update: 2020-07-13
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Source: Internet
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Author: User
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In cancer, the common receptor tyrosine kinase (PTKs) is expressed or mutated, and PTKs are involved in driving tumor growth and metastasisIn modern PTK signaling models (including MET), downstream phosphatidyl inositol inositol 3-kinase (PI3K) mediates cell proliferation and cell migration, while the birds glycese (GTPase) Rac1 mediates cell migrationbut in cultured NIH3T3 and glioblastoma cells, Hervieu et alfound that type I PI3K led to tumor MET-induced cell migration, but did not affect the growth of anchornon dependenceInstead, Rac1 regulates both processes in different waysdownstream as PI3K, Rac1 uses its GTPase active mediated cell migration without relying on PI3K, and Rac1 uses the function of the adapter to mediate the anchoring of non-dependent cell growth in gtPase-dependent mannerform a compound through its RKR molds, Rac1 and kinase mTOR to facilitate the translocation of its tomatic membrane, while its activity promotes the non-dependent growth of the anchoring of cultured cellsInhibition of mTOR with rapamycin inhibits the growth of cell grafts with subcutaneous MET mutations in mice, as well as cells that are resistant to MET inhibitorsthese findings reveal the role of Rac1 in the gtPase non-dependency in the mediated PI3K non-dependent MET-mTOR pathway, and suggests alternative or joint strategies that can overcome resistance to RTK inhibitors in cancer patients
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