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Activation of PI3K/PKB Signaling in Breast Cancer May Inhibit TGF-Beta- Induced G1 Arrest Through Changes in p27 Function

机译:乳腺癌中pI3K / pKB信号的激活可通过p27功能的变化抑制TGF-β诱导的G1期逮捕

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Loss of responsiveness to TGF-beta-induced cell cycle inhibition is a hallmark of cancers and the underlying mechanisms are not well understood. We now show PKB activation contributes to resistance to antiproliferative signals including TGF-beta and breast cancer progression in part by impairing nuclear import and action of p27. We observed in TGF-beta resistant human mammary epithelial cells, PKB is overactivated and p27 is mislocalized in the cytoplasm and the nuclear localization of p27 can be restored by PI3K inhibition. PKB transfection caused cytoplasmic p27 accumulation and resistance to cytokine- mediated G1 arrest.

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