AIM: To investigate the expression of p57kip2 and its relationship with clinicopathology, PCNA and p53 in primary hepatocellular carcinoma (HCC). METHODS: Expression of p57kip2, PCNA and p53 in tumor tissues from 32 p...AIM: To investigate the expression of p57kip2 and its relationship with clinicopathology, PCNA and p53 in primary hepatocellular carcinoma (HCC). METHODS: Expression of p57kip2, PCNA and p53 in tumor tissues from 32 patients with HCC and 10 liver tissues of normal persons was detected with Elivision immunohistochemical technique. RESULTS: The p57kip2 protein positive-expression rate in HCC was 56.25%, lower than that in normal tissues (100%, P<0.05). The reduced expression of p57kip2 protein correlated significantly with moderate or low differentiation of tumor cells (P = 0.007 <0.05), high clinical stage (P= 0.041 <0.05) and poor prognosis (P= 0.036 <0.05), but did not correlate significantly with metastasis, tumor size, level of AFP and age (P>0.05). The PCNA positive-expression rate was 56.25%, which was correlated significantly with the expression of p57kip2 (P= 0.025<0.05). The p53 positive-expression rate was 46.88%, which was not correlated significantly with the expression of p57kip2 (P>0.05). CONCLUSION: There is a marked loss or absence of p57kip2 expression and high expression of PCNA in HCC, which are involved in carcinogenesis and development of HCC. The p57kip2 and p53 may induce apoptosis via different mechanisms.展开更多
背景与目的:原发性胆囊癌(primary carcinoma of the gallbladder,PCG)是死亡率极高的恶性肿瘤,其恶变的机制目前尚未明确。前期研究发现,p57^(KIP2)在人类多种恶性肿瘤中异常表达。本研究拟进一步探讨p57^(KIP2)在PCG组织中的表达及临...背景与目的:原发性胆囊癌(primary carcinoma of the gallbladder,PCG)是死亡率极高的恶性肿瘤,其恶变的机制目前尚未明确。前期研究发现,p57^(KIP2)在人类多种恶性肿瘤中异常表达。本研究拟进一步探讨p57^(KIP2)在PCG组织中的表达及临床意义。方法:运用实时荧光定量聚合酶链反应(real-time fluorescence quantitative polymerase chain reaction,RTFQ-PCR)、免疫组织化学EliVision法分别检测60例PCG、20例胆囊腺瘤(adenoma of the gallbladder,AG)和20例慢性胆囊炎(chronic cholecystitis,CC)组织中p57^(KIP2)、cyclin D1、cyclin E mRNA表达及蛋白水平。结果:p57^(KIP2) mRNA及蛋白在PCG、AG和CC中的表达逐渐升高,两两比较差异有统计学意义(P<0.05)。Cyclin D1、cyclin E mRNA及蛋白在PCG、AG和CC中的表达逐渐降低,PCG与AG比较、PCG与CC比较,差异有统计学意义(P<0.05)。在PCG组织中,p57^(KIP2)蛋白的表达与临床分期、组织学分级及淋巴结转移有关(P<0.05)。Cyclin D1蛋白的表达与临床分期有关(P<0.05)。p57^(KIP2)与cyclin D1的表达呈负相关(P<0.05),p57^(KIP2)与cyclin E的表达呈负相关(P<0.05),cyclin D1与cyclin E的表达呈正相关(P<0.05)。结论:p57^(KIP2)表达的降低与cyclin D1、cyclin E表达的增加可能是PCG的发生机制之一;检测p57^(KIP2)、cyclin D1及cyclin E对PCG的预后判断有重要意义。展开更多
【目的】研究p57kip2基因在人肝细胞癌(hepatocellular carcinoma,HCC)不同阶段的杂合性缺失(loss of heterozygosity,LOH),以探讨HCC发生的分子生物学机制。【方法】运用PCR聚丙烯酰胺凝胶电泳-银染法对30例肝癌组织p57kip2基因位点上...【目的】研究p57kip2基因在人肝细胞癌(hepatocellular carcinoma,HCC)不同阶段的杂合性缺失(loss of heterozygosity,LOH),以探讨HCC发生的分子生物学机制。【方法】运用PCR聚丙烯酰胺凝胶电泳-银染法对30例肝癌组织p57kip2基因位点上2个微卫星位点(TH01和D11S2359)进行LOH的检测。【结果】30例肝癌组织中有9例至少在1个微卫星位点(30.0%)表现出LOH,且分化好肝癌组织LOH率明显低于和分化差肝癌组织。【结论】p57kip2基因位点频繁的LOH在HCC发生中起重要作用。展开更多
目的探讨癌基因△Np63对膀胱癌细胞增殖和凋亡的影响,并初步探讨其可能的分子机制。方法通过将△Np63特异性短发夹RNA(△Np63-shRNA)和非特异性短发夹RNA(Control-shRNA)转染膀胱移行细胞癌(transitional cell carcinom a of bladder,TC...目的探讨癌基因△Np63对膀胱癌细胞增殖和凋亡的影响,并初步探讨其可能的分子机制。方法通过将△Np63特异性短发夹RNA(△Np63-shRNA)和非特异性短发夹RNA(Control-shRNA)转染膀胱移行细胞癌(transitional cell carcinom a of bladder,TCCB)5637细胞,用半定量逆转录-聚合酶链反应(RT-PCR)和Westernblot分别检测△Np63、p27kip1、p57kip2mRNA和蛋白的表达水平,WST-1法检测细胞增殖活性,利用流式细胞术(FCM)检测细胞周期分布,TUNEL法检测细胞凋亡情况。结果特异性的△Np63-shRNA能够有效地沉默△Np63并上调p27kip1和p57kip2的基因和蛋白水平,转染△Np63-shRNA的5637细胞的增殖能力明显受到抑制(P<0.05),且明显促进了细胞的凋亡(P<0.05)。结论靶向△Np63基因的shRNA片段可以有效的抑制人膀胱癌5637细胞的增殖并促进其凋亡,其可能的机制是通过上调p27kip1和p57kip2的表达实现的。展开更多
文摘AIM: To investigate the expression of p57kip2 and its relationship with clinicopathology, PCNA and p53 in primary hepatocellular carcinoma (HCC). METHODS: Expression of p57kip2, PCNA and p53 in tumor tissues from 32 patients with HCC and 10 liver tissues of normal persons was detected with Elivision immunohistochemical technique. RESULTS: The p57kip2 protein positive-expression rate in HCC was 56.25%, lower than that in normal tissues (100%, P<0.05). The reduced expression of p57kip2 protein correlated significantly with moderate or low differentiation of tumor cells (P = 0.007 <0.05), high clinical stage (P= 0.041 <0.05) and poor prognosis (P= 0.036 <0.05), but did not correlate significantly with metastasis, tumor size, level of AFP and age (P>0.05). The PCNA positive-expression rate was 56.25%, which was correlated significantly with the expression of p57kip2 (P= 0.025<0.05). The p53 positive-expression rate was 46.88%, which was not correlated significantly with the expression of p57kip2 (P>0.05). CONCLUSION: There is a marked loss or absence of p57kip2 expression and high expression of PCNA in HCC, which are involved in carcinogenesis and development of HCC. The p57kip2 and p53 may induce apoptosis via different mechanisms.
文摘背景与目的:原发性胆囊癌(primary carcinoma of the gallbladder,PCG)是死亡率极高的恶性肿瘤,其恶变的机制目前尚未明确。前期研究发现,p57^(KIP2)在人类多种恶性肿瘤中异常表达。本研究拟进一步探讨p57^(KIP2)在PCG组织中的表达及临床意义。方法:运用实时荧光定量聚合酶链反应(real-time fluorescence quantitative polymerase chain reaction,RTFQ-PCR)、免疫组织化学EliVision法分别检测60例PCG、20例胆囊腺瘤(adenoma of the gallbladder,AG)和20例慢性胆囊炎(chronic cholecystitis,CC)组织中p57^(KIP2)、cyclin D1、cyclin E mRNA表达及蛋白水平。结果:p57^(KIP2) mRNA及蛋白在PCG、AG和CC中的表达逐渐升高,两两比较差异有统计学意义(P<0.05)。Cyclin D1、cyclin E mRNA及蛋白在PCG、AG和CC中的表达逐渐降低,PCG与AG比较、PCG与CC比较,差异有统计学意义(P<0.05)。在PCG组织中,p57^(KIP2)蛋白的表达与临床分期、组织学分级及淋巴结转移有关(P<0.05)。Cyclin D1蛋白的表达与临床分期有关(P<0.05)。p57^(KIP2)与cyclin D1的表达呈负相关(P<0.05),p57^(KIP2)与cyclin E的表达呈负相关(P<0.05),cyclin D1与cyclin E的表达呈正相关(P<0.05)。结论:p57^(KIP2)表达的降低与cyclin D1、cyclin E表达的增加可能是PCG的发生机制之一;检测p57^(KIP2)、cyclin D1及cyclin E对PCG的预后判断有重要意义。
文摘【目的】研究p57kip2基因在人肝细胞癌(hepatocellular carcinoma,HCC)不同阶段的杂合性缺失(loss of heterozygosity,LOH),以探讨HCC发生的分子生物学机制。【方法】运用PCR聚丙烯酰胺凝胶电泳-银染法对30例肝癌组织p57kip2基因位点上2个微卫星位点(TH01和D11S2359)进行LOH的检测。【结果】30例肝癌组织中有9例至少在1个微卫星位点(30.0%)表现出LOH,且分化好肝癌组织LOH率明显低于和分化差肝癌组织。【结论】p57kip2基因位点频繁的LOH在HCC发生中起重要作用。
文摘目的探讨癌基因△Np63对膀胱癌细胞增殖和凋亡的影响,并初步探讨其可能的分子机制。方法通过将△Np63特异性短发夹RNA(△Np63-shRNA)和非特异性短发夹RNA(Control-shRNA)转染膀胱移行细胞癌(transitional cell carcinom a of bladder,TCCB)5637细胞,用半定量逆转录-聚合酶链反应(RT-PCR)和Westernblot分别检测△Np63、p27kip1、p57kip2mRNA和蛋白的表达水平,WST-1法检测细胞增殖活性,利用流式细胞术(FCM)检测细胞周期分布,TUNEL法检测细胞凋亡情况。结果特异性的△Np63-shRNA能够有效地沉默△Np63并上调p27kip1和p57kip2的基因和蛋白水平,转染△Np63-shRNA的5637细胞的增殖能力明显受到抑制(P<0.05),且明显促进了细胞的凋亡(P<0.05)。结论靶向△Np63基因的shRNA片段可以有效的抑制人膀胱癌5637细胞的增殖并促进其凋亡,其可能的机制是通过上调p27kip1和p57kip2的表达实现的。
