【摘 要】
：
喉癌发病率位于耳鼻喉恶性肿瘤的第二位,约占全身肿瘤的1％～5％.肽基脯氨酰顺反异构酶(PIN1)可催化磷酸化的丝/苏-脯氨酸肽键发生顺反异构,异常表达与肿瘤形成有关,影响肿瘤细
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喉癌发病率位于耳鼻喉恶性肿瘤的第二位,约占全身肿瘤的1％～5％.肽基脯氨酰顺反异构酶(PIN1)可催化磷酸化的丝/苏-脯氨酸肽键发生顺反异构,异常表达与肿瘤形成有关,影响肿瘤细胞的生物学行为.核转录因子κB (NF-κB)的五个成员过激活在多种人类癌症中都有被发现.而细胞周期蛋白依赖激酶2(CDK2)在细胞增殖中起重要作用,是肿瘤细胞增殖的限速蛋白.深入探讨PIN1经NF-KB通路上调CDK2表达对喉癌细胞系Hep-2生物学行为影响,有助于解释喉癌的发生发展分子机制.喉癌细胞系Hep-2经PIN1过表达载体(pcDNA3.1-PIN1)、NF-κB抑制剂(BAY11-7082)、PIN1的siRNA及NF-kB激活剂(IL-1 β)处理后,免疫荧光实验检测中心体分裂异常,流式细胞仪检测细胞周期和凋亡,克隆形成、CCK-8检测细胞增殖,划痕和Transwell实验检测肿瘤细胞的迁移及侵袭能力,免疫荧光和Western-blot检测NF-κB/p65入核情况,RT-PCR和Western-blot检测PIN1对CDK2的表达的影响.研究表明,PIN1过表达促进中心体异常增殖、克隆形成、增加细胞迁移侵袭、细胞周期G1/S转化,NF-κB/p65入核以及CDK2的表达,并且可以通过NF-kB的抑制剂消减上述影响.沉默PIN1表达后,抑制中心体异常增殖、克隆形成、细胞迁移侵袭、细胞增殖、细胞周期G1/S的转化、NF-κB/p65入核以及CDK2的表达,而且通过NF-kB激活剂逆转这些作用.综上所述,PIN1经NF-κB通路上调CDK2表达影响Hep-2细胞的生物学行为,为揭示喉癌的发生发展初制提供了实验基础.
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