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首页> 外文期刊>Molecular and Cellular Biology >Overexpression of core-binding factor alpha (CBF alpha) reverses cellular transformation by the CBF beta-smooth muscle myosin heavy chain chimeric oncoprotein.
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Overexpression of core-binding factor alpha (CBF alpha) reverses cellular transformation by the CBF beta-smooth muscle myosin heavy chain chimeric oncoprotein.

机译：核心结合因子α（CBF alpha）的过表达逆转了CBFβ-平滑肌肌球蛋白重链嵌合癌蛋白的细胞转化。

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A fusion between the transcription factor core-binding factor beta (CBF beta; also known as PEBP2 beta) and the tail region of smooth muscle myosin heavy chain (SMMHC) is generated by an inversion of chromosome 16 [inv(16) (p13q22)] associated with the M4Eo subtype of acute myeloid leukemia. We have previously shown that this CBF beta-SMMHC chimeric protein can transform NIH 3T3 cells and that this process requires regions of the chimeric protein necessary for association with the CBF alpha subunit. In this study, we show that NIH 3T3 cells overexpressing murine Cbf alpha 2 (also known as Aml1) cannot be transformed by CBF beta-SMMHC and that overexpression of Cbf alpha 2 in cells previously transformed by CBF beta-SMMHC reverts the cells to a less transformed phenotype. Cbf alpha 2 overexpression does not cause any gross morphological changes to NIH 3T3 cells but does result in increased CBF activity, as indicated by electrophoretic mobility shift assays and transactivation of reporter constructs. Cells transformed by CBF beta-SMMHC lack normal CBF-DNA complexes and have decreased levels of transactivation. Reversion of CBF beta-SMMHC transformation by Cbf alpha 2 is associated with a restoration of normal CBF-DNA complexes and transactivation activity. A Cbf alpha 2 mutant lacking transactivation properties does not transform cells when overexpressed, nor does it protect cells from CBF beta-SMMHC transformation. These results suggest that CBF beta-SMMHC interferes with the normal function of CBF and that this interference is necessary but not sufficient for cellular transformation.
机译：转录因子核心结合因子beta（CBF beta;也称为PEBP2 beta）与平滑肌肌球蛋白重链（SMMHC）的尾巴区域之间的融合是通过16号染色体的反转[inv（16）（p13q22） ]与急性髓细胞性白血病的M4Eo亚型相关。先前我们已经表明，这种CBFβ-SMMHC嵌合蛋白可以转化NIH 3T3细胞，并且此过程需要与CBFα亚基缔合所必需的嵌合蛋白区域。在这项研究中，我们表明过表达鼠类Cbf alpha 2（也称为Aml1）的NIH 3T3细胞不能被CBF beta-SMMHC转化，而先前由CBF beta-SMMHC转化的细胞中Cbf alpha 2的过表达会将细胞还原为转化表型较少。 Cbf alpha 2的过表达不会引起NIH 3T3细胞的总体形态变化，但会导致CBF活性增加，如电泳迁移率迁移分析和报告基因构建体的反式激活所示。由CBFβ-SMMHC转化的细胞缺乏正常的CBF-DNA复合物，反式激活水平降低。 Cbf alpha 2还原CBF beta-SMMHC转化与正常CBF-DNA复合物和反式激活活性的恢复有关。缺乏反式激活特性的Cbf alpha 2突变体在过表达时不会转化细胞，也不会保护细胞免受CBF beta-SMMHC转化。这些结果表明，CBF beta-SMMHC干扰CBF的正常功能，并且这种干扰对于细胞转化是必要的，但还不足以实现。

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