目的检测鼻腔鼻窦内翻性乳头状瘤中上皮细胞膜蛋白1(EMP1)、环氧化酶2(COX-2)及Stathmin蛋白的表达情况,分析其与上皮化生程度的相关性。方法选取2015年1月~2016年3月在本院就诊的鼻腔鼻窦内翻性乳头状瘤患者28例作为实验组,20例肥厚性...目的检测鼻腔鼻窦内翻性乳头状瘤中上皮细胞膜蛋白1(EMP1)、环氧化酶2(COX-2)及Stathmin蛋白的表达情况,分析其与上皮化生程度的相关性。方法选取2015年1月~2016年3月在本院就诊的鼻腔鼻窦内翻性乳头状瘤患者28例作为实验组,20例肥厚性鼻炎患者的下鼻甲黏膜组织作为对照组,采用免疫组化技术和q RT-PCR检测鼻腔鼻窦内翻性乳头状瘤、下鼻甲黏膜组织EMP1、COX-2以及Stathmin的表达情况,并比较三种因子在不同组织中的表达情况。结果实验组EMP1蛋白表达的阳性率显著低于对照组(P<0.05),COX-2及Stathmin蛋白表达的阳性率显著高于对照组(P<0.05)。实验组EMP1的m RNA水平显著低于对照组(P<0.05),COX-2及Stathmin m RNA水平显著高于对照组(P<0.05)。EMP1蛋白表达水平与上皮化生的严重程度呈负相关,COX-2及Stathmin蛋白表达水平与上皮化生的严重程度呈正相关。结论鼻腔鼻窦内翻性乳头状瘤中EMP1、COX-2及Stathmin蛋白的异常表达与上皮化生程度有关,联合检测EMP1、COX-2及Stathmin蛋白表达可评估鼻腔鼻窦内翻性乳头状瘤上皮异常重塑情况。展开更多
This study examined the role of EMP-1 in tumorigenesis of non-small cell lung carcinoma (NSCLC) and the possible mechanism. Specimens were collected from 28 patients with benign lung diseases and 28 with NSCLC, and im...This study examined the role of EMP-1 in tumorigenesis of non-small cell lung carcinoma (NSCLC) and the possible mechanism. Specimens were collected from 28 patients with benign lung diseases and 28 with NSCLC, and immunohis to chemically detected to evaluate the correlation of EMP-1 expression to the clinical features of NSCLC. Recombinant adenovirus was constructed to over-express EMP-1 and then infect PC9 cells. Cell proliferation was measured by Ki67 staining. Western blotting was performed to examine the effect of EMP-1 on the PI3K/AKT signaling. Moreover, tumor xeno-grafts were established by subcutaneous injection of PC9 cell suspension (about 5×107/mL in 100 μL of PBS) into the right hind limbs of athymic nude mice. The results showed EMP-1 was significantly up-regulated in NSCLC patients as compared with those with benign lung diseases. Over-expression of EMP-1 promoted proliferation of PC9 cells, which coincided with the activation of the PI3K/AKT pathway. EMP-1 promoted the growth of xenografts of PC9 cells in athymic nude mice. It was concluded that EMP-1 expression may contribute to the development and progress of NSCLC by activating PI3K/AKT pathway.展开更多
文摘目的检测鼻腔鼻窦内翻性乳头状瘤中上皮细胞膜蛋白1(EMP1)、环氧化酶2(COX-2)及Stathmin蛋白的表达情况,分析其与上皮化生程度的相关性。方法选取2015年1月~2016年3月在本院就诊的鼻腔鼻窦内翻性乳头状瘤患者28例作为实验组,20例肥厚性鼻炎患者的下鼻甲黏膜组织作为对照组,采用免疫组化技术和q RT-PCR检测鼻腔鼻窦内翻性乳头状瘤、下鼻甲黏膜组织EMP1、COX-2以及Stathmin的表达情况,并比较三种因子在不同组织中的表达情况。结果实验组EMP1蛋白表达的阳性率显著低于对照组(P<0.05),COX-2及Stathmin蛋白表达的阳性率显著高于对照组(P<0.05)。实验组EMP1的m RNA水平显著低于对照组(P<0.05),COX-2及Stathmin m RNA水平显著高于对照组(P<0.05)。EMP1蛋白表达水平与上皮化生的严重程度呈负相关,COX-2及Stathmin蛋白表达水平与上皮化生的严重程度呈正相关。结论鼻腔鼻窦内翻性乳头状瘤中EMP1、COX-2及Stathmin蛋白的异常表达与上皮化生程度有关,联合检测EMP1、COX-2及Stathmin蛋白表达可评估鼻腔鼻窦内翻性乳头状瘤上皮异常重塑情况。
基金supported by grants from the National Natural Science Foundation of China (Nos.81072431,30872472,30973496 and 30800569)the Innovative Foundation of Huazhong University of Science and Technology (No.2010MS027)+1 种基金the Foundation of "973" Program (No.2009CB521802)by Special Fund for Central University Basic Scientific Research (Nos.2011JC062,2011JC063)
文摘This study examined the role of EMP-1 in tumorigenesis of non-small cell lung carcinoma (NSCLC) and the possible mechanism. Specimens were collected from 28 patients with benign lung diseases and 28 with NSCLC, and immunohis to chemically detected to evaluate the correlation of EMP-1 expression to the clinical features of NSCLC. Recombinant adenovirus was constructed to over-express EMP-1 and then infect PC9 cells. Cell proliferation was measured by Ki67 staining. Western blotting was performed to examine the effect of EMP-1 on the PI3K/AKT signaling. Moreover, tumor xeno-grafts were established by subcutaneous injection of PC9 cell suspension (about 5×107/mL in 100 μL of PBS) into the right hind limbs of athymic nude mice. The results showed EMP-1 was significantly up-regulated in NSCLC patients as compared with those with benign lung diseases. Over-expression of EMP-1 promoted proliferation of PC9 cells, which coincided with the activation of the PI3K/AKT pathway. EMP-1 promoted the growth of xenografts of PC9 cells in athymic nude mice. It was concluded that EMP-1 expression may contribute to the development and progress of NSCLC by activating PI3K/AKT pathway.
