Inhibition of mammalian target of rapamycin signaling potentiates the effects of all-trans retinoic acid to induce growth arrest and differentiation of human acute myelogenous leukemia cells.
作者： Chie Nishioka , Takayuki Ikezoe , Jing Yang , Sigal Gery , H. Phillip Koeffler
DOI: 10.1002/IJC.24472
关键词: Endocrinology 、 Tretinoin 、 HL60 、 Cancer research 、 Cell growth 、 Cell cycle 、 Biology 、 Cell culture 、 Cellular differentiation 、 mTORC1 、 Retinoic acid 、 Internal medicine
摘要: Our study explored the drug interaction of all-trans retinoic acid (ATRA) and RAD001 (everolimus), inhibitor mammalian target rapamycin complex 1 (mTORC1), in acute myelogenous leukemia (AML) NB4 HL60 cells. (10 nM) significantly enhanced ATRA-induced growth arrest differentiation these cells, as measured by colony-forming assay cell cycle analysis, expression CD11b surface antigen nitroblue tetrazolium reduction, respectively. ATRA (0.1-1 microM) upregulated levels RTP801, a negative regulator mTORC1, inhibited mTORC1 signaling assessed measurement p-p70S6K p-4E-BP1 combination with strikingly downregulated p-70S6K without affecting total amount proteins. Notably, augmented CCAAT/enhancer-binding protein epsilon (C/EBPepsilon) p27(kip1) c-Myc Furthermore, (5 mg/kg) ability to inhibit proliferation cells growing tumor xenografts immune-deficient nude mice. Taken together, concomitant blockade RA may be promising treatment strategy for individuals AML.
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