Suppression of oncogenic properties of c-Myc by LKB1-controlled epithelial organization.
作者： J. I. Partanen , A. I. Nieminen , T. P. Makela , J. Klefstrom
关键词:
摘要: Cellular organization into epithelial architecture maintains structural integrity and homeostasis by suppressing cell proliferation apoptosis. However, it is unclear whether the sufficient to block induction of cell-autonomous cycle progression apoptotic sensitivity activated oncogenes. We show that chronic activation oncogenic c-Myc, starting in developing 3D organotypic mammary acinar structures, results hyperproliferation transformed morphology. Surprisingly, acute c-Myc mature quiescent acini with established fails reinitiate or transform these structures. does quiescent, but structurally unorganized, acini, which demonstrates proper needed for blockade. The capability structures also restored loss LKB1, a human homologue polarity protein PAR4. restrains activity coactivation complementary TNF-related apoptosis-inducing ligand death receptor pathway can induce strong Bim Bid-mediated response acini. together expose surprising apoptosis resistance organized identify role regulator LKB1 development c-Myc-resistant organization.
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