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作 者:赵朋月[1] 宋建[2] 刁路明[1] 罗小青[2] 黄燕华 王则胜[4] 陈洪雷[1]
机构地区:[1]武汉大学基础医学院病理学教研室,湖北武汉430071 [2]湖北医药学院附属襄阳市第一人民医院肿瘤科,湖北襄阳441000 [3]武汉市肿瘤纳米诊断工程技术研究中心分子病理科,湖北武汉430070 [4]武汉大学人民医院病理科,湖北武汉430060
出 处:《肿瘤》2012年第9期731-737,共7页Tumor
基 金:国家自然科学基金资助项目(编号:30900652)
摘 要:目的:检测基质Cav-1(caveolin-1)、M2型丙酮酸激酶(pyruvate kinase M2,PKM2)和左旋乳酸脱氢酶B(L-lactate dehydrogenase B,LDH-B)在人肺腺癌(pulmonary adenocarcinoma,PAC)组织中的表达,探讨基质Cav-1对PAC侵袭和转移的影响。方法:利用量子点免疫荧光组织化学技术检测68例PAC组织和16例非癌变肺组织中基质Cav-1、LDH-B和PKM2的表达,同时应用量子点免疫荧光双标法检测基质Cav-1和α-平滑肌肌动蛋白(α-smooth muscle actin,α-SMA)的共表达。结果:基质Cav-1、LDH-B和PKM2在PAC组织中的阳性表达率分别为58.8%、54.4%和35.3%,在非癌变肺组织中的阳性表达率分别为100.0%、12.5%和6.3%,差异有统计学意义(P<0.05)。Cav-1、LDH-B和PKM2蛋白的表达与PAC患者的临床病理参数无相关性(P>0.05)。基质Cav-1与LDH-B和PKM2蛋白的表达呈负相关(P<0.05,r_s=-0.406;P<0.05,r_s=-0.320),基质LDH-B与PKM2蛋白的表达之间呈正相关(P<0.05,r_s=0.367)。结论:基质Cav-1表达缺失可能促进PAC的形成,其机制可能与上调LDH-B和PKM2的表达有关。Objective: To examime the expressions of caveolin-1 (Cav-1), pyruvate kinase M2 (PKM2) and L-lactate dehydrogenase B (LDH-B) proteins in human pulmonary adenocarcinoma (PAC) tissues, and to investigate the effect of stromal Cav-1 expression on the invasion and metastasis of PAC. Methods: The expressions of stromal Cav-1, LDH-B and PKM2 proteins in PAC tissues from 68 cases and non-cancerous lung tissues from 16 cases were detected by quantum dots-based immunofluorescent histochemistry, and the co-expressions of stromal Cav-1 and α-smooth muscle actin (α-SMA) proteins were detected by quantum dots-based double-labeling immunofluorescence method. Results: The positive rates of stromal Cav-1, LDH-B and PKM2 expression were 58.8%, 54.4% and 35.3% in the PAC tissues, respectively, while which were 100%, 12.5% and 6.3% in the non-cancerous lung tissues, respectively. The difference between PAC and non-cancerous lung tissues was significant (P 〈 0.05). There was no significant relationship between the expressions of stromal Cav-1, LDH-B and PKM2 proteins and the clinicopathological characteristics of patients with PAC (P 〉 0.05). The expression of stromal Cav-1 was negatively correlated with the expressions of stromal LDH-B and PKM2 (P 〈 0.05, rs = –0.406; P 〈 0.05, rs = –0.320), but the expression of stromal LDH-B was positively correlated with the expression of stromal PKM2 (P 〈 0.05, rs = 0.367). Conclusion: The loss of stromal Cav-1 expression may promote PAC formation, and this mechanism may be associated with the up-regulation of LDH-B and PKM2 expressions.
关 键 词:肺肿瘤 能量代谢 量子点 癌相关成纤维细胞 CAVEOLIN-1
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