肿瘤转移消失蛋白(missing in metastasis,MIM)是一种新近发现的肌动蛋白结合蛋白,主要参与细胞骨架的重塑、信号转导及转录活化,与肿瘤的生长和侵袭密切相关。近年来,该蛋白在不同肿瘤中作用机制的研究受到广泛关注,有着广阔的研究前...肿瘤转移消失蛋白(missing in metastasis,MIM)是一种新近发现的肌动蛋白结合蛋白,主要参与细胞骨架的重塑、信号转导及转录活化,与肿瘤的生长和侵袭密切相关。近年来,该蛋白在不同肿瘤中作用机制的研究受到广泛关注,有着广阔的研究前景。本文通过综述MIM蛋白与肿瘤发生发展的相关性,从而为MIM蛋白在肿瘤诊断和治疗中的应用提供理论基础及新的策略。展开更多
目的:探讨CXCR4／CXCL12在结直肠癌肝转移中的作用．方法:应用Western blot检测160例结直肠癌患者标本中肿瘤组织、邻近正常黏膜以及肝转移组织中CXCR4／CXCL12通路成员的表达情况,免疫组织化学法检测CXCR4／CXCL12在细胞水平的分布．结...目的:探讨CXCR4／CXCL12在结直肠癌肝转移中的作用．方法:应用Western blot检测160例结直肠癌患者标本中肿瘤组织、邻近正常黏膜以及肝转移组织中CXCR4／CXCL12通路成员的表达情况,免疫组织化学法检测CXCR4／CXCL12在细胞水平的分布．结果:与正常组织相比,结直肠癌组织中 CXCR4／CXCL12表达水平明显增高(P<0．05); 与原发肿瘤相比,10例肝转移组织中CXCR4／ CXCL12表达增高(CXCR4:3．9±0．5 vs 2．2± 0．3,P<0．05:CXCL12:3．6±0．5 vs 2．4±0．3, P<0．05):TNMⅢ、Ⅳ分期CXCR4／CXCL12表达水平比Ⅰ、Ⅱ分期显著增加有关(CXCR4: 3．4±0．6 vs 1．8±0．3．P<0．05;CXCL12:3．6± 0．5 vs 1．8±0．4．P<0．05)．结论:趋化因子受体CXCR4／CXCL12在原发结直肠癌与肝转移组织中呈高表达,CXCR4／ CXCL12信号转导通路可能在结直肠癌肝转移过程中起一定作用．展开更多
The most frequent cause of death for cancer patients is metastasis. The precise molecular events leading to the acquisition of malignant phenotypes remain largely unknown. During the past 10 years, we have focused our...The most frequent cause of death for cancer patients is metastasis. The precise molecular events leading to the acquisition of malignant phenotypes remain largely unknown. During the past 10 years, we have focused our efforts on exploring signaling mechanisms underlying malignant progression of human prostate carcinoma. We found that activation of P2Y purinoceptor on androgen independent prostate carcinoma cell lines resulted in significant growth inhibition. This growth inhibitory effect was accompanied by activation of phospholipase C and calcium mobilization, and proved receptor specific. We also demonstrated that the G protein coupled P2Y purinoceptor was linked to Erk1/2 and p38 MAPK pathway, and there existed cross talk between phospholipase C and MAPK pathways. We found Erk1/2 and p38 MAPK pathways were differentially activated between metastatic and non metastatic prostate carcinoma cell subclones, providing valuable clue to further study molecular mechanism of tumor metastasis.展开更多
文摘肿瘤转移消失蛋白(missing in metastasis,MIM)是一种新近发现的肌动蛋白结合蛋白,主要参与细胞骨架的重塑、信号转导及转录活化,与肿瘤的生长和侵袭密切相关。近年来,该蛋白在不同肿瘤中作用机制的研究受到广泛关注,有着广阔的研究前景。本文通过综述MIM蛋白与肿瘤发生发展的相关性,从而为MIM蛋白在肿瘤诊断和治疗中的应用提供理论基础及新的策略。
文摘目的:探讨CXCR4／CXCL12在结直肠癌肝转移中的作用．方法:应用Western blot检测160例结直肠癌患者标本中肿瘤组织、邻近正常黏膜以及肝转移组织中CXCR4／CXCL12通路成员的表达情况,免疫组织化学法检测CXCR4／CXCL12在细胞水平的分布．结果:与正常组织相比,结直肠癌组织中 CXCR4／CXCL12表达水平明显增高(P<0．05); 与原发肿瘤相比,10例肝转移组织中CXCR4／ CXCL12表达增高(CXCR4:3．9±0．5 vs 2．2± 0．3,P<0．05:CXCL12:3．6±0．5 vs 2．4±0．3, P<0．05):TNMⅢ、Ⅳ分期CXCR4／CXCL12表达水平比Ⅰ、Ⅱ分期显著增加有关(CXCR4: 3．4±0．6 vs 1．8±0．3．P<0．05;CXCL12:3．6± 0．5 vs 1．8±0．4．P<0．05)．结论:趋化因子受体CXCR4／CXCL12在原发结直肠癌与肝转移组织中呈高表达,CXCR4／ CXCL12信号转导通路可能在结直肠癌肝转移过程中起一定作用．
文摘The most frequent cause of death for cancer patients is metastasis. The precise molecular events leading to the acquisition of malignant phenotypes remain largely unknown. During the past 10 years, we have focused our efforts on exploring signaling mechanisms underlying malignant progression of human prostate carcinoma. We found that activation of P2Y purinoceptor on androgen independent prostate carcinoma cell lines resulted in significant growth inhibition. This growth inhibitory effect was accompanied by activation of phospholipase C and calcium mobilization, and proved receptor specific. We also demonstrated that the G protein coupled P2Y purinoceptor was linked to Erk1/2 and p38 MAPK pathway, and there existed cross talk between phospholipase C and MAPK pathways. We found Erk1/2 and p38 MAPK pathways were differentially activated between metastatic and non metastatic prostate carcinoma cell subclones, providing valuable clue to further study molecular mechanism of tumor metastasis.
