目的：通过凋膜止崩液对人离体子宫内膜增生症（EH）腺上皮细胞PTEN、Rb2/p130基因表达的影响,探讨其对EH的治疗机理。方法：分离、培养30例原代人子宫内膜增生症（EH）腺上皮细胞并采用CK-19鉴定,将纯化后的腺上皮细胞随机分为4组：空...目的：通过凋膜止崩液对人离体子宫内膜增生症（EH）腺上皮细胞PTEN、Rb2/p130基因表达的影响,探讨其对EH的治疗机理。方法：分离、培养30例原代人子宫内膜增生症（EH）腺上皮细胞并采用CK-19鉴定,将纯化后的腺上皮细胞随机分为4组：空白对照组、凋膜止崩液大剂量组（50μg/mL）、凋膜止崩液中剂量组（25μg/mL）、凋膜止崩液小剂量组（12.5μg/mL）,分别于用药24、48、72 h观察下列指标的变化：四甲基偶氮噻唑兰（MTT）法检测3个时间点各组细胞的增殖率、实时定量聚合酶连反应（RT-PCR）以及Western blot分别检测各组细胞PTEN、Rb2/p130 m RNA及蛋白表达的差异。结果：与空白对照组比较,凋膜止崩液各组腺上皮细胞的增殖率明显降低,且呈时间和剂量依赖性（P〈0.05）;凋膜止崩液组EH腺上皮细胞中PTEN、Rb2/p130 m RNA及蛋白的表达明显增加,与空白对照组相比差异显著（P〈0.05）。结论：凋膜止崩液能明显抑制EH腺上皮细胞的增殖,其抑制作用与上调细胞抑癌基因PTEN、Rb2/p130的表达有关。展开更多
Deregulation of the cell cycle results in loss of normal control mechanisms that prevent aberrant cell proliferation and cancer progression. Regulation of the cell cycle is a highly complex process with many layers of...Deregulation of the cell cycle results in loss of normal control mechanisms that prevent aberrant cell proliferation and cancer progression. Regulation of the cell cycle is a highly complex process with many layers of control. One of these mechanisms involves timely degradation of CDK inhibitors (CKIs) like p27Kip1 by the ubiquitin proteasomal system (UPS). Cks1 is a 9 kDa protein which is frequently overexpressed in different tumor subtypes, and has pleiotropic roles in cell cycle progression, many of which remain to be fully characterized. One well characterized molecular role of Cks1 is that of an essential adaptor that regulates p27Kip1 abundance by facilitating its interaction with the SCF-Skp2 E3 ligase which appends ubiquitin to p27Kip1 and targets it for degradation through the UPS. In addition, emerging research has uncovered p27Kip1-independent roles of Cks1 which have provided crucial insights into how it may be involved in cancer progression. We review here the structural features of Cks1 and their functional implications, and also some recently identified Cks1 roles and their involvement in breast and other cancers.展开更多
文摘目的：通过凋膜止崩液对人离体子宫内膜增生症（EH）腺上皮细胞PTEN、Rb2/p130基因表达的影响,探讨其对EH的治疗机理。方法：分离、培养30例原代人子宫内膜增生症（EH）腺上皮细胞并采用CK-19鉴定,将纯化后的腺上皮细胞随机分为4组：空白对照组、凋膜止崩液大剂量组（50μg/mL）、凋膜止崩液中剂量组（25μg/mL）、凋膜止崩液小剂量组（12.5μg/mL）,分别于用药24、48、72 h观察下列指标的变化：四甲基偶氮噻唑兰（MTT）法检测3个时间点各组细胞的增殖率、实时定量聚合酶连反应（RT-PCR）以及Western blot分别检测各组细胞PTEN、Rb2/p130 m RNA及蛋白表达的差异。结果：与空白对照组比较,凋膜止崩液各组腺上皮细胞的增殖率明显降低,且呈时间和剂量依赖性（P〈0.05）;凋膜止崩液组EH腺上皮细胞中PTEN、Rb2/p130 m RNA及蛋白的表达明显增加,与空白对照组相比差异显著（P〈0.05）。结论：凋膜止崩液能明显抑制EH腺上皮细胞的增殖,其抑制作用与上调细胞抑癌基因PTEN、Rb2/p130的表达有关。
文摘Deregulation of the cell cycle results in loss of normal control mechanisms that prevent aberrant cell proliferation and cancer progression. Regulation of the cell cycle is a highly complex process with many layers of control. One of these mechanisms involves timely degradation of CDK inhibitors (CKIs) like p27Kip1 by the ubiquitin proteasomal system (UPS). Cks1 is a 9 kDa protein which is frequently overexpressed in different tumor subtypes, and has pleiotropic roles in cell cycle progression, many of which remain to be fully characterized. One well characterized molecular role of Cks1 is that of an essential adaptor that regulates p27Kip1 abundance by facilitating its interaction with the SCF-Skp2 E3 ligase which appends ubiquitin to p27Kip1 and targets it for degradation through the UPS. In addition, emerging research has uncovered p27Kip1-independent roles of Cks1 which have provided crucial insights into how it may be involved in cancer progression. We review here the structural features of Cks1 and their functional implications, and also some recently identified Cks1 roles and their involvement in breast and other cancers.
